P-selectin deficiency exacerbates experimental glomerulonephritis: a protective role for endothelial P-selectin in inflammation.

@article{Rosenkranz1999PselectinDE,
  title={P-selectin deficiency exacerbates experimental glomerulonephritis: a protective role for endothelial P-selectin in inflammation.},
  author={Alexander R. Rosenkranz and Donna L. Mendrick and Ramzi S. Cotran and Tanya Norton Mayadas},
  journal={The Journal of clinical investigation},
  year={1999},
  volume={103 5},
  pages={649-59}
}
P-selectin is a leukocyte adhesion receptor present in endothelial cells and platelets. We examined the role of P-selectin in the autologous phase of an accelerated model of anti-glomerular basement membrane (GBM) glomerulonephritis using P-selectin-deficient mice and chimeric mice expressing P-selectin only in platelets or endothelial cells. P-selectin-deficient mice exhibited more severe glomerular damage with increased interstitial mononuclear leukocytic infiltrates, and had significantly… CONTINUE READING

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P - selectin is a leukocyte adhesion receptor present in endothelial cells and platelets .
P - selectin is a leukocyte adhesion receptor present in endothelial cells and platelets .
P - selectin is a leukocyte adhesion receptor present in endothelial cells and platelets .
P - selectin is a leukocyte adhesion receptor present in endothelial cells and platelets .
P - selectin deficiency exacerbates experimental glomerulonephritis : a protective role for endothelial P - selectin in inflammation .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
P - selectin deficiency exacerbates experimental glomerulonephritis : a protective role for endothelial P - selectin in inflammation .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Thus , the protective effect in wild - type mice may be accounted for , in part by soluble P - selectin shed by non - renal endothelial cells , although other endothelial P - selectin - dependent mechanisms can not be ruled out .
Thus , the protective effect in wild - type mice may be accounted for , in part by soluble P - selectin shed by non - renal endothelial cells , although other endothelial P - selectin - dependent mechanisms can not be ruled out .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
P - selectin deficiency exacerbates experimental glomerulonephritis : a protective role for endothelial P - selectin in inflammation .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
P - selectin deficiency exacerbates experimental glomerulonephritis : a protective role for endothelial P - selectin in inflammation .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Thus , the protective effect in wild - type mice may be accounted for , in part by soluble P - selectin shed by non - renal endothelial cells , although other endothelial P - selectin - dependent mechanisms can not be ruled out .
Thus , the protective effect in wild - type mice may be accounted for , in part by soluble P - selectin shed by non - renal endothelial cells , although other endothelial P - selectin - dependent mechanisms can not be ruled out .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
P - selectin deficiency exacerbates experimental glomerulonephritis : a protective role for endothelial P - selectin in inflammation .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
P - selectin deficiency exacerbates experimental glomerulonephritis : a protective role for endothelial P - selectin in inflammation .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Thus , the protective effect in wild - type mice may be accounted for , in part by soluble P - selectin shed by non - renal endothelial cells , although other endothelial P - selectin - dependent mechanisms can not be ruled out .
Thus , the protective effect in wild - type mice may be accounted for , in part by soluble P - selectin shed by non - renal endothelial cells , although other endothelial P - selectin - dependent mechanisms can not be ruled out .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
P - selectin deficiency exacerbates experimental glomerulonephritis : a protective role for endothelial P - selectin in inflammation .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
P - selectin deficiency exacerbates experimental glomerulonephritis : a protective role for endothelial P - selectin in inflammation .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Thus , the protective effect in wild - type mice may be accounted for , in part by soluble P - selectin shed by non - renal endothelial cells , although other endothelial P - selectin - dependent mechanisms can not be ruled out .
Thus , the protective effect in wild - type mice may be accounted for , in part by soluble P - selectin shed by non - renal endothelial cells , although other endothelial P - selectin - dependent mechanisms can not be ruled out .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
P - selectin is a leukocyte adhesion receptor present in endothelial cells and platelets .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
Thus , the protective effect in wild - type mice may be accounted for , in part by soluble P - selectin shed by non - renal endothelial cells , although other endothelial P - selectin - dependent mechanisms can not be ruled out .
P - selectin deficiency exacerbates experimental glomerulonephritis : a protective role for endothelial P - selectin in inflammation .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
P - selectin deficiency exacerbates experimental glomerulonephritis : a protective role for endothelial P - selectin in inflammation .
Thus , the protective effect in wild - type mice may be accounted for , in part by soluble P - selectin shed by non - renal endothelial cells , although other endothelial P - selectin - dependent mechanisms can not be ruled out .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
P - selectin on the endothelium was predominantly responsible for protection from the exacerbated disease , because chimeric mice with endothelial P - selectin , and not mice with platelet P - selectin , showed glomerular injury similar to that in wild - type animals .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
Thus , the protective effect in wild - type mice may be accounted for , in part by soluble P - selectin shed by non - renal endothelial cells , although other endothelial P - selectin - dependent mechanisms can not be ruled out .
P - selectin deficiency exacerbates experimental glomerulonephritis : a protective role for endothelial P - selectin in inflammation .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
Levels of soluble circulating P - selectin were increased in nephritic wild - type mice and in chimeric mice with endothelial P - selectin , but not platelet P - selectin .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
We examined the role of P - selectin in the autologous phase of an accelerated model of anti - glomerular basement membrane ( GBM ) glomerulonephritis using P - selectin - deficient mice and chimeric mice expressing P - selectin only in platelets or endothelial cells .
P - selectin deficiency exacerbates experimental glomerulonephritis : a protective role for endothelial P - selectin in inflammation .
Thus , the protective effect in wild - type mice may be accounted for , in part by soluble P - selectin shed by non - renal endothelial cells , although other endothelial P - selectin - dependent mechanisms can not be ruled out .
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