RhoA required for acid-induced stress fiber formation and trafficking and activation of NHE3.

@article{Yang2007RhoARF,
  title={RhoA required for acid-induced stress fiber formation and trafficking and activation of NHE3.},
  author={Xiaojing Yang and Hai-chang Huang and Helen L. Yin and Robert J. Alpern and Patricia A. Preisig},
  journal={American journal of physiology. Renal physiology},
  year={2007},
  volume={293 4},
  pages={
          F1054-64
        }
}
Exposure to an acid load increases apical membrane Na(+)/H(+) antiporter (NHE3) activity, a process that involves exocytic trafficking of the transporter to the apical membrane. We have previously shown that an intact microfilament structure is required for this exocytic process (Yang X, Amemiya M, Peng Y, Moe OW, Preisig PA, Alpern RJ. Am J Physiol Cell Physiol 279: C410-C419, 2000). The present studies demonstrate that acid-induced stress fiber formation is required for stimulation of NHE3… 
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Lysophosphatidic acid stimulation of NHE3 exocytosis in polarized epithelial cells occurs with release from NHERF2 via ERK-PLC-PKCδ signaling.
TLDR
LPA stimulation of N HE3 exocytosis includes a signaling pathway that regulates fixation of NHE3 to the MV cytoskeleton, which involves a signaling module consisting of ERK-PLC-PKCδ, which dynamically and reversibly releases NHE 3 from NHERF2 to contribute to the changes in NHE2 MV mobility.
The calcineurin homologous protein-1 increases Na(+)/H(+) -exchanger 3 trafficking via ezrin phosphorylation.
TLDR
It is found that overexpression of the calcineurin homologous protein-1 (CHP1) in opossum kidney cells increased NHE3 transport activity, surface protein abundance, and ezrin phosphorylation, and CHP1 knockdown by small interfering RNA had the opposite effects.
Dual roles for RHOA/RHO-kinase in the regulated trafficking of a voltage-sensitive potassium channel.
TLDR
Temperature block experiments show that ROCK affects cholesterol-dependent trafficking by modulating the recycling of endocytosed channel back to the plasma membrane, indicating a key role for actin remodeling in RhoA-dependent Kv1.2 regulation.
Rho rocks H⁺-ATPases. Focus on "Regulation of V-ATPase recycling via a RhoA- and ROCKII-dependent pathway in epididymal clear cells".
  • C. Wagner
  • Biology
    American journal of physiology. Cell physiology
  • 2011
TLDR
It is revealed that clear cell H-ATPases have a critical role in regulating the pH of the luminal fluid where sperm is stored and the acidic environment in the epididymis prevents premature activation.
The acid-activated signaling pathway: starting with Pyk2 and ending with increased NHE3 activity.
TLDR
The acid-activated signaling pathway in the proximal tubule that senses a decrease in cell pH and then mediates stimulation of the apical membrane Na/H antiporter, isoform NHE3 is discussed.
Lysophosphatidic acid 5 receptor induces activation of Na(+)/H(+) exchanger 3 via apical epidermal growth factor receptor in intestinal epithelial cells.
TLDR
The results unveil a pivotal role of apical EGFR in NHE3 regulation by LPA and show that the RhoA-ROCK-Pyk2 and MEK-ERK pathways converge onto N HE3.
High-mobility group box 1 inhibits HCO3- absorption in the medullary thick ascending limb through RAGE-Rho-ROCK-mediated inhibition of basolateral Na+/H+ exchange.
TLDR
It is concluded that HMGB1 inhibits HCO3 (-) absorption in the MTAL through a RAGE-RhoA-ROCK1 signaling pathway coupled to inhibition of NHE1.
Endothelin-1 Augments Na+/H+ Exchange Activity in Murine Pulmonary Arterial Smooth Muscle Cells via Rho Kinase
TLDR
The results indicate that ET-1 can modulate pH homeostasis in PASMCs via a signaling pathway that includes Rho kinase and that, in contrast to systemic vascular smooth muscle, activation of PKC does not appear to be an important regulator of PAS MC pHi.
Acid regulation of NaDC-1 requires a functional endothelin B receptor.
TLDR
The acid-activated pathway mediating stimulation of NaDC-1 activity requires a functional ET(B) receptor in vivo and in vitro, as does acid stimulation of NHE3 activity, which indicates that there are similarities in the signaling pathway mediates these responses.
High-mobility group box 1 inhibits HCO 3 absorption in the medullary thick ascending limb through RAGE-Rho-ROCK-mediated inhibition of basolateral Na / H exchange
TLDR
It is concluded that HMGB1 inhibits HCO3 absorption in the MTAL through a RAGE-RhoA-ROCK1 signaling pathway coupled to inhibition of NHE1.
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References

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TLDR
Pyk2 may serve as the pH sensor that initiates the acid-regulated signaling cascade involved in NHE3 regulation, given that partially purified Pyk2 can be activated by acid in a cell-free system.
Overexpression of csk inhibits acid-induced activation of NHE-3.
TLDR
It is shown that decreases in pH activate c-src and that the src family nonreceptor protein-tyrosine kinases play a key role in acid activation of NHE-3.
In response to protein load podocytes reorganize cytoskeleton and modulate endothelin-1 gene: implication for permselective dysfunction of chronic nephropathies.
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TLDR
In OKPETB6 cells, a clonal cell line of OKP cells that overexpresses ETB receptors, ET-1-induced increases in Na+/H+ antiporter activity are mediated50% by Ca2(+)-dependent pathways and 50% by tyrosine kinase pathways.
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TLDR
Optimal NHE3 activity requires a functional RhoA-ROK signaling pathway which acts, at least partly, by controlling the phosphorylation of myosin light chain and, ultimately, the organization of the actin cytoskeleton.
Acid incubation causes exocytic insertion of NHE3 in OKP cells.
TLDR
Two mechanisms for acid-induced increases in NHE3 activity are demonstrated: Beginning at 6 h, there is an increase in apical membrane NHE2 that is due to stimulated exocytic insertion and is required for increased N HE3 activity, and at 24 h,there is an additional increase in total cellular Nhe3.
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TLDR
Testing the effect of actin-modifying agents on NHE3 activity found that inhibition of transport was not due to diminution in the number of transporters at the plasmalemma, suggesting a physical interaction of exchangers with the cytoskeleton.
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TLDR
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ET(B) receptor activation causes exocytic insertion of NHE3 in OKP cells.
TLDR
It is demonstrated that ET-1 induces net trafficking of NHE3 to the apical membrane that is mediated by enhanced exocytic insertion and is required for increased NHE 3 activity.
Inhibition of Rho-Kinase Reduces Renal Na-H Exchanger Activity and Causes Natriuresis in Rat
TLDR
It is concluded that apical NHE activity is increased in SHR PCT compared with controls and that inhibition of Rho-kinase reduces PCT NHE activities and causes natriuresis.
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