PACAP (pituitary adenylate cyclase-activating polypeptide) occurs in two biologically active forms, with 38 and 37 amino acid residues (PACAP38 and PACAP27). In mammalian tissues, PACAP38 is the dominant form. Diverse effects have been described in the cardiovascular, respiratory, gastrointestinal, and urogenital systems. PACAP is known for its strong cytoprotective effects, which are present endogenously as well, as proven by knockout studies and results showing that PACAP is up-regulated following diverse injuries. Little is known about such effects in the kidney. We have previously shown that PACAP is protective in renal ischemia-reperfusion injury. Therefore, the aim of the present study was to investigate the changes of endogenous PACAP following 60-minute renal ischemia using radioimmunoassay. Changes were observed within 24 hours following renal vessel clamping. In the cortex, an acute decrease was followed by an increase on the intact side, and levels returned to original ones on the operated side. In the medulla, changes were only observed on the clamped side: a marked up-regulation was detected in PACAP38-like immunoreactivity within the first 24 hours. The present study showed that PACAP38- and PACAP27-like immunoreactivities sensitively react to renal ischemia-reperfusion, the physiological importance of which awaits further investigation.
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http://dx.doi.org/10.1016/j.transproceed.2010.05.012 | DOI Listing |
Anal Chem
January 2025
Anhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
The absence of an effective imaging tool for diagnosing renal ischemia-reperfusion injury (RIRI) severely delays its treatment, and currently, no definitive clinical interventions are available. Pyroglutamate aminopeptidase-1 (PGP-1), a potential inflammatory cytokine, has shown considerable potential as a biomarker for tracing the inflammatory process in vivo. However, its exact role in the enhanced visualization of RIRI in complex biological systems has yet to be fully established.
View Article and Find Full Text PDFAppl Biochem Biotechnol
January 2025
Department of Nephrology, Affiliated Hospital of Youjiang Medical University for Nationalities, 18Th Zhongshan 2Nd Road, Baise, 533000, Guangxi, China.
A growing body of evidence suggests the involvement of long noncoding ribose nucleic acids (lncRNAs) in acute kidney injury (AKI). This study focused on the mechanistic role of lncRNA small nucleolar RNA host gene 12 (SNHG12) in ischemia/reperfusion (I/R)-mediated AKI. A model of hypoxia/reoxygenation (H/R) was created using human kidney cells (HK-2).
View Article and Find Full Text PDFMol Biotechnol
January 2025
The First Affiliated Hospital of Hebei North University Address, 12 Changqing Road, Zhangjiakou City, Hebei Province, China.
Renal ischemia-reperfusion injury (RIRI) is a primary cause of acute kidney injury (AKI), frequently resulting in high mortality rates and progression to chronic kidney disease (CKD). This study aimed to investigate the therapeutic potential of total saponins from Panax notoginseng (PNS) in the context of RIRI. Utilizing a murine RIRI model, the efficacy of PNS was evaluated, demonstrating a significant reduction in renal inflammation and cellular pyroptosis.
View Article and Find Full Text PDFMol Immunol
January 2025
Department of Urology, Renmin Hospital of Wuhan University. Wuhan, Hubei Province, PR China. Electronic address:
Background: Renal ischemia-reperfusion injury (IRI) is a prevailing manifestation of acute kidney injury (AKI) with limited treatment options. TRIM44 has emerged as a possible target for treatment due to its regulatory function in inflammatory pathways.
Methods: In vivo and in vitro models were employed to ascertain the TRIM44 impact on renal IRI.
FASEB J
January 2025
Department of Urology, Capital Medical University Beijing Chaoyang Hospital, Beijing, China.
Podocytes are essential to maintain the normal filtration function of glomerular basement membrane, which could be injured by ischemia-reperfusion. As complicated function of autophagy in terminal differentiated podocytes, autophagy dysfunction might contribute to I/R induced renal dysfunction following glomerular filtration membrane (GFM) injuries. Meanwhile, apelin-13, an endogenous polypeptide, has been proved to be effective in regulating autophagy and apoptosis in podocytes.
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