5-HT1f receptor regulates mitochondrial homeostasis and its loss potentiates acute kidney injury and impairs renal recovery

Whitney S. Gibbs, Justin B. Collier, Morgan Morris, Craig C. Beeson, Judit Megyesi, Rick G. Schnellmann

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

Our laboratory previously reported that agonists of the 5-hydoxytryptam-ine 1F (5-HT1F) receptor induce renal mitochondrial biogenesis (MB) and that stimulation of the 5-HT1F receptor following ischemia/ reperfusion (I/R)-induced acute kidney injury (AKI) accelerated the recovery of renal function in mice. The goal of this study was to examine the contribution of the 5-HT1F receptor in the regulation of renal mitochondrial homeostasis and renal function in naïve and injured mice. Although 5-HT1F receptor knockout (KO) mice were healthy and fertile, and did not exhibit renal dysfunction, renal mitochondrial DNA copy number and mitochondrial fission gene expression increased at 10 wk of age. The 5-HT1F receptor KO mice exhibited greater proximal tubular injury and diminished renal recovery after I/R-induced AKI compared with wild-type mice. These findings were associated with persistent suppression of renal cortical MB and ATP levels after injury. In summary, the 5-HT1F receptor is a component of physiological MB regulation in the kidney, and its absence potentiates renal injury and impedes recovery.

Original languageEnglish (US)
Pages (from-to)F1119-F1128
JournalAmerican Journal of Physiology - Renal Physiology
Volume315
Issue number4
DOIs
StatePublished - Oct 5 2018

Keywords

  • Acute kidney injury
  • Gene expression
  • Mitochondria
  • Serotonin

ASJC Scopus subject areas

  • Physiology
  • Urology

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