Author pages are created from data sourced from our academic publisher partnerships and public sources.
Share This Author
CCN3 (NOV) is a negative regulator of CCN2 (CTGF) and a novel endogenous inhibitor of the fibrotic pathway in an in vitro model of renal disease.
Both CCN2 and CCN3 appear to act in a yin/yang manner to regulate ECM metabolism, which may serve to naturally limit fibrosis in vivo and provide opportunities for novel, endogenous-based therapeutic treatments.
Pathogenesis of Experimental Hypertension Produced by Carotid Sinus Area Constriction in Dogs
- E. Crandall, H. L. McCrorey, E. Sukowski, G. Wakerlin
- Medicine, BiologyCirculation research
- 1 November 1957
Bilateral constriction of the carotid sinus area, the immediate arterial branches of the sinus, or (perhaps) the vertebral arteries, and bilateral resection of the carotid sinus produces a…
Glucose transport by isolated plasma membranes of the bovine blood-brain barrier.
- W. J. Lee, D. Peterson, E. Sukowski, R. Hawkins
- Biology, ChemistryThe American journal of physiology
- 1 May 1997
The abluminal Na-dependent glucose transporter is in a position to transport glucose from the brain extracellular fluid into the endothelial cells of the blood-brain barrier, providing a mechanism for glucose movement between blood and brain.
CCN3/CCN2 regulation and the fibrosis of diabetic renal disease
- B. Riser, F. Najmabadi, D. Peterson
- Biology, MedicineJournal of Cell Communication and Signaling
- 9 February 2010
The results corroborate the hypothesis that one function of CCN3 is to regulate CCN2 activity and at the concentrations and conditions used down-regulates the effects of TGF-β1, acting to limit ECM turnover and fibrosis in vivo.
Activation of proximal tubular Na(+)-H+ exchange by angiotensin II.
The data indicate that the Vmax effect is caused by an apparent increase in the number (density) of active Na(+)-H+ carriers present in the luminal membrane, and the possibility that the observed kinetic change involves an exocytic mechanism was tested.
Treatment with the matricellular protein CCN3 blocks and/or reverses fibrosis development in obesity with diabetic nephropathy.
Blood–Brain Barrier Transport Pathways for Cytoprotective Thiols
Findings are consistent with the presence of a typical &ggr;-glutamyl cycle at the luminal membrane of BBB endothelial cells, a significant efflux pathway at the abluminal membrane allowing passive movement ofBBB GSH into brain extracellular fluid, a Na-dependent, brain-to-blood pathway for transcellular transport of GSH, and a mechanism for cytoprotection under conditions of ischemia and reperfusion.
ACCUMULATION OF POLYGLUCOSIDES IN ANAEROBIC RAT LIVER.
In Vitro Studies on Degradation of Gamma-L-Glutamyl-L-Cysteine and Gamma-L-Glutamyl-D-Cysteine in Blood: Implications for Treatment of Stroke
- N. Ikpa, R. Forman, K. Garchow, E. Sukowski, D. Peterson
- Biology, MedicineAmerican journal of therapeutics
- 1 July 2015
It is shown that &ggR;-Glu-Cys remains intact in blood for several minutes, and the analog &ggr;- Glu-D-CYS may be a more stable, but similarly effective antioxidant.