Effect of kidney ischemia/reperfusion injury on proliferation, apoptosis, and cellular senescence in acute kidney injury in mice.

Autor:	Sari FT; Universitas Gadjah Mada, Public Health, and Nursing, Faculty of Medicine, Department of Anatomy, Jl. Farmako Sekip Utara, Yogyakarta, Indonesia., Sari FT; Universitas Gadjah Mada, Public Health, and Nursing, Faculty of Medicine, Postgraduate Programs of Biomedical Science, Jl. Farmako Sekip Utara, Yogyakarta, Indonesia., Sari FT; Universitas Gadjah Mada, Faculty of Dentistry, Jl. Farmako Sekip Utara, Yogyakarta, Indonesia., Arfian N; Universitas Gadjah Mada, Public Health, and Nursing, Faculty of Medicine, Department of Anatomy, Jl. Farmako Sekip Utara, Yogyakarta, Indonesia. nur_arfian@ugm.ac.id., Sari DCR; Universitas Gadjah Mada, Public Health, and Nursing, Faculty of Medicine, Department of Anatomy, Jl. Farmako Sekip Utara, Yogyakarta, Indonesia.
Jazyk:	angličtina
Zdroj:	The Medical journal of Malaysia [Med J Malaysia] 2020 May; Vol. 75 (Suppl 1), pp. 20-23.
Abstrakt:	Introduction: Kidney ischemia/reperfusion injury (IRI) is the leading cause of acute kidney injury (AKI). Kidney IRI demonstrated apoptosis of epithelial cells in acute phase followed by proliferation of interstitial cells in chronic episode, and cellular senescence may contribute to development of AKI, however, its occurrence within acute or chronic episodes is still not completely understood. Methods: Kidney IRI was performed with bilateral pediculus clamping in Swiss Background mice (3 months, 30-40g). Mice were euthanised on day one (I/R1, n=6), day eight (I/R8, n=6), and day twelve (I/R12, n=6) to exam acute and chronic episodes. Sham operation procedure was performed in the control. Tubular injury was assessed based on periodic acid- Schift (PAS) staining. Reverse transcriptase PCR (RT-PCR) was done to quantify mRNA expression of Bax, Bcl-2, and p16. Immunohistostaining (IHC) was performed to examine localisation of apoptosis (p53) and proliferation (Bcl-2). Results: RT-PCR analysis showed upregulation of mRNA expression of Bcl-2, Bax, and p16 (p<0.05). The data showed that ischemia/reperfusion induces upregulation of Bax (p=0.20), Bcl-2 (p=0.45), p16 (p=0.18). Apoptosis and proliferation occurred in the epithelial cells in acute episodes, but occurred in interstitial areas in chronic episodes. Conclusions: Ischemia/reperfusion injury induces upregulation proliferation, apoptosis, and cellular senescence in acute kidney injury. Apoptosis reached its peak on day 1, proliferation on day 8, and cellular senescence on day 12.
Databáze:	MEDLINE
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