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Absence of PKCα Alters the Renal Immune Response in Angiotensin II‐dependent Hypertension
Author(s) -
Borchart Matthew R.,
Pulous Fadi E.,
Wang Yirong,
Sun Michael A.,
Himmel Nathaniel J.,
Vanderford Thomas H.,
Blount Mitsi A.
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.969.17
Subject(s) - endocrinology , medicine , immune system , kidney , angiotensin ii , protein kinase c , cytokine , renin–angiotensin system , t cell , cd8 , stimulation , chemistry , blood pressure , immunology , signal transduction , biochemistry
Angiotensin II (Ang II) stimulation of T‐cell proliferation and accumulation plays an important role in the development of hypertension and end‐stage kidney damage. Unfortunately, the signaling mechanisms behind the immune response within the kidney remains underexplored. One pathway that is important to both Ang II and T‐cell response is mediated by PKCα. To determine the role of PKCα in facilitating T‐cell infiltration in the kidney during Ang II‐dependent hypertension, PKCα null (KO) mice were treated with either saline or Ang II and compared to PKCα control (WT) mice treated similarly. After 14 days, systolic blood pressure, water intake and urine output were increased in all Ang II‐treated mice. Kidney damage and collagen deposition is elevated with ANG II treatment and appears more extensive in KO mice. Ang II‐treatment significantly increased spleen weight in WT mice only; suggesting that the absence of PKCα attenuates increased immune cell production. Histological examination of immune cell infiltration of the renal cortex revealed that Ang II‐treatment increased CD4+ and CD8+ T‐cells but not macrophage invasion in both WT and KO mice and suggests that CD4+ T‐cell recruitment is higher in Ang II‐treated WT compared to treated KO mice. Immune cell infiltration and cytokine production was also measured via flow cytometry and results suggest that PKCα is important for Ang II‐meditated cytokine release in renal tissues. Collectively, these data suggest that the absence of PKCα decreases inflammatory response to Ang II‐induced hypertension in the kidney. Support or Funding Information NIDDK R25‐DK101390