In Vivo Tracking of Mesenchymal Stem Cell-Derived Extracellular Vesicles Improving Mitochondrial Function in Renal Ischemia–Reperfusion Injury

ACS Nano ◽  
2020 ◽  
Vol 14 (4) ◽  
pp. 4014-4026 ◽  
Author(s):  
Hongmei Cao ◽  
Yuanqiu Cheng ◽  
Heqi Gao ◽  
Jie Zhuang ◽  
Weiguang Zhang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Reperfusion Injury ◽  
Extracellular Vesicles ◽  
Mitochondrial Function ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury

scholarly journals In vivo mechanism study of NGAL in rat renal ischemia-reperfusion injury

2014 ◽  
Vol 13 (4) ◽  
pp. 8740-8748 ◽  
Author(s):  
X.J. Zang ◽  
S.X. An ◽  
Z. Feng ◽  
Y.P. Xia ◽  
Y. Song ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Mechanism Study ◽  
Renal Ischemia Reperfusion Injury

scholarly journals HDAC2 targeting stabilizes the CoREST complex in renal tubular cells and protects against renal ischemia/reperfusion injury

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
David D. Aufhauser ◽  
Paul Hernandez ◽  
Seth J. Concors ◽  
Ciaran O’Brien ◽  
Zhonglin Wang ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Tubules ◽  
Renal Protection ◽  
Renal Tubular Cells ◽  
Renal Ischemia Reperfusion Injury ◽  
Renal Tubular

AbstractHistone/protein deacetylases (HDAC) 1 and 2 are typically viewed as structurally and functionally similar enzymes present within various co-regulatory complexes. We tested differential effects of these isoforms in renal ischemia reperfusion injury (IRI) using inducible knockout mice and found no significant change in ischemic tolerance with HDAC1 deletion, but mitigation of ischemic injury with HDAC2 deletion. Restriction of HDAC2 deletion to the kidney via transplantation or PAX8-controlled proximal renal tubule-specific Cre resulted in renal IRI protection. Pharmacologic inhibition of HDAC2 increased histone acetylation in the kidney but did not extend renal protection. Protein analysis demonstrated increased HDAC1-associated CoREST protein in HDAC2-/- versus WT cells, suggesting that in the absence of HDAC2, increased CoREST complex occupancy of HDAC1 can stabilize this complex. In vivo administration of a CoREST inhibitor exacerbated renal injury in WT mice and eliminated the benefit of HDAC2 deletion. Gene expression analysis of endothelin showed decreased endothelin levels in HDAC2 deletion. These data demonstrate that contrasting effects of HDAC1 and 2 on CoREST complex stability within renal tubules can affect outcomes of renal IRI and implicate endothelin as a potential downstream mediator.

MP41-02 PROPHYLAXIS AGAINST RENAL ISCHEMIA REPERFUSION INJURY IN CANINE MODEL: STEM CELL APPROACH.

2017 ◽  
Vol 197 (4S) ◽  
Author(s):  
Yasser Osman ◽  
Sahar M. Hamed ◽  
Nashwa Barakat ◽  
Sherry Khater ◽  
Mahmoud Gabr ◽  
...  
Keyword(s):  
Stem Cell ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Canine Model ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury
Sign in / Sign up

Export Citation Format

Share Document