Bcl-2 19-kDa Interacting Protein 3 (BNIP3)-Mediated Mitophagy Attenuates Intermittent Hypoxia-Induced Human Renal Tubular Epithelial Cell Injury

BACKGROUND As a novel pathophysiological characteristic of obstructive sleep apnea, intermittent hypoxia (IH) contributes to human renal tubular epithelial cells impairment. The underlying pathological mechanisms remain unrevealed. The present study aimed to evaluate the influence of Bcl-2 19-kDa in...

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Veröffentlicht in:Medical science monitor 2022-07, Vol.28, p.e936760-e936760
Hauptverfasser: Zhang, Xiao-Bin, Chen, Gong-Ping, Huang, Mao-Hong, Chen, Xiang-Xing, Zhan, Feng-Fu, He, Xiu-Zhen, Cai, Ling, Zeng, Hui-Qing
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container_title Medical science monitor
container_volume 28
creator Zhang, Xiao-Bin
Chen, Gong-Ping
Huang, Mao-Hong
Chen, Xiang-Xing
Zhan, Feng-Fu
He, Xiu-Zhen
Cai, Ling
Zeng, Hui-Qing
description BACKGROUND As a novel pathophysiological characteristic of obstructive sleep apnea, intermittent hypoxia (IH) contributes to human renal tubular epithelial cells impairment. The underlying pathological mechanisms remain unrevealed. The present study aimed to evaluate the influence of Bcl-2 19-kDa interacting protein 3 (BNIP3)-mediated mitophagy on IH-induced renal tubular epithelial cell impairment. MATERIAL AND METHODS Human kidney proximal tubular (HK-2) cells were exposed to IH condition. IH cycles were as follows: 21% oxygen for 25 min, 21% descended to 1% for 35 min, 1% oxygen sustaining for 35 min, and 1% ascended to 21% for 25 min. The IH exposure lasted 24 h with 12 cycles of hypoxia and re-oxygenation. Both the siBNIP3 and BNIP3 vector were transfected to cells. Cell viability and apoptosis, mitochondrial morphology and function, and mitophagy were detected by cell counting kit-8, flow cytometry and TUNEL staining, transmission electron microscopy, western blotting, and immunofluorescence, respectively. RESULTS In the IH-induced HK-2 cells, inhibition of BNIP3 further aggravated mitochondrial structure damage, and decreased mitophagy level, leading to increased cell apoptosis and decreased cell viability. While overexpression of BNIP3 enhanced mitophagy, which protected mitochondrial structure, it can decrease cell death in HK-2 cells exposed to IH. CONCLUSIONS The present study showed that BNIP3-mediated mitophagy plays a protective role against IH-induced renal tubular epithelial cell impairment.
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The underlying pathological mechanisms remain unrevealed. The present study aimed to evaluate the influence of Bcl-2 19-kDa interacting protein 3 (BNIP3)-mediated mitophagy on IH-induced renal tubular epithelial cell impairment. MATERIAL AND METHODS Human kidney proximal tubular (HK-2) cells were exposed to IH condition. IH cycles were as follows: 21% oxygen for 25 min, 21% descended to 1% for 35 min, 1% oxygen sustaining for 35 min, and 1% ascended to 21% for 25 min. The IH exposure lasted 24 h with 12 cycles of hypoxia and re-oxygenation. Both the siBNIP3 and BNIP3 vector were transfected to cells. Cell viability and apoptosis, mitochondrial morphology and function, and mitophagy were detected by cell counting kit-8, flow cytometry and TUNEL staining, transmission electron microscopy, western blotting, and immunofluorescence, respectively. RESULTS In the IH-induced HK-2 cells, inhibition of BNIP3 further aggravated mitochondrial structure damage, and decreased mitophagy level, leading to increased cell apoptosis and decreased cell viability. While overexpression of BNIP3 enhanced mitophagy, which protected mitochondrial structure, it can decrease cell death in HK-2 cells exposed to IH. CONCLUSIONS The present study showed that BNIP3-mediated mitophagy plays a protective role against IH-induced renal tubular epithelial cell impairment.</description><identifier>ISSN: 1643-3750</identifier><identifier>ISSN: 1234-1010</identifier><identifier>EISSN: 1643-3750</identifier><identifier>DOI: 10.12659/MSM.936760</identifier><identifier>PMID: 35836356</identifier><language>eng</language><publisher>United States: International Scientific Literature, Inc</publisher><subject>Apoptosis ; Epithelial Cells - metabolism ; Humans ; Hypoxia - metabolism ; Lab/In Vitro Research ; Membrane Proteins - metabolism ; Mitophagy - physiology ; Oxygen - metabolism ; Proto-Oncogene Proteins - metabolism</subject><ispartof>Medical science monitor, 2022-07, Vol.28, p.e936760-e936760</ispartof><rights>Med Sci Monit, 2022 2022</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-bd7ec7c41349a1c3c3f5ff1ddcd4232e2904d0edfc876267e909bec2d55aec1b3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9295414/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9295414/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35836356$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Xiao-Bin</creatorcontrib><creatorcontrib>Chen, Gong-Ping</creatorcontrib><creatorcontrib>Huang, Mao-Hong</creatorcontrib><creatorcontrib>Chen, Xiang-Xing</creatorcontrib><creatorcontrib>Zhan, Feng-Fu</creatorcontrib><creatorcontrib>He, Xiu-Zhen</creatorcontrib><creatorcontrib>Cai, Ling</creatorcontrib><creatorcontrib>Zeng, Hui-Qing</creatorcontrib><title>Bcl-2 19-kDa Interacting Protein 3 (BNIP3)-Mediated Mitophagy Attenuates Intermittent Hypoxia-Induced Human Renal Tubular Epithelial Cell Injury</title><title>Medical science monitor</title><addtitle>Med Sci Monit</addtitle><description>BACKGROUND As a novel pathophysiological characteristic of obstructive sleep apnea, intermittent hypoxia (IH) contributes to human renal tubular epithelial cells impairment. The underlying pathological mechanisms remain unrevealed. The present study aimed to evaluate the influence of Bcl-2 19-kDa interacting protein 3 (BNIP3)-mediated mitophagy on IH-induced renal tubular epithelial cell impairment. MATERIAL AND METHODS Human kidney proximal tubular (HK-2) cells were exposed to IH condition. IH cycles were as follows: 21% oxygen for 25 min, 21% descended to 1% for 35 min, 1% oxygen sustaining for 35 min, and 1% ascended to 21% for 25 min. The IH exposure lasted 24 h with 12 cycles of hypoxia and re-oxygenation. Both the siBNIP3 and BNIP3 vector were transfected to cells. Cell viability and apoptosis, mitochondrial morphology and function, and mitophagy were detected by cell counting kit-8, flow cytometry and TUNEL staining, transmission electron microscopy, western blotting, and immunofluorescence, respectively. RESULTS In the IH-induced HK-2 cells, inhibition of BNIP3 further aggravated mitochondrial structure damage, and decreased mitophagy level, leading to increased cell apoptosis and decreased cell viability. While overexpression of BNIP3 enhanced mitophagy, which protected mitochondrial structure, it can decrease cell death in HK-2 cells exposed to IH. CONCLUSIONS The present study showed that BNIP3-mediated mitophagy plays a protective role against IH-induced renal tubular epithelial cell impairment.</description><subject>Apoptosis</subject><subject>Epithelial Cells - metabolism</subject><subject>Humans</subject><subject>Hypoxia - metabolism</subject><subject>Lab/In Vitro Research</subject><subject>Membrane Proteins - metabolism</subject><subject>Mitophagy - physiology</subject><subject>Oxygen - metabolism</subject><subject>Proto-Oncogene Proteins - metabolism</subject><issn>1643-3750</issn><issn>1234-1010</issn><issn>1643-3750</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUU1v1DAQjRAV_YATd-RjUZXij9hZX5DapbArdWlVytly7MmuS-Kkjo3Yf8FPxrBtVU4zevPmzRu9onhL8CmhgssPq2-rU8lELfCL4oCIipWs5vjls36_OJymO4zpTGD-qthnfMYE4-Kg-H1uupIiIssfnzRa-ghBm-j8Gl2HIYLziKHj86_La_a-XIF1OoJFKxeHcaPXW3QWI_iUwWm327u_QESL7Tj8crpceptM3likXnt0A1536DY1qdMBXYwubqBzGZpD12WBuxS2r4u9VncTvHmoR8X3zxe380V5efVlOT-7LA2bkVg2tgZTm4qwSmpimGEtb1tirbEVZRSoxJXFYFszqwUVNUgsGzDUcq7BkIYdFR93umNqerAmuw66U2NwvQ5bNWin_p94t1Hr4aeSVPKKVFng-EEgDPcJpqh6N5n8iPYwpElRIQnmFHOZqSc7qgnDNAVon84QrP5lqHKGapdhZr977uyJ-xga-wOqHZlm</recordid><startdate>20220715</startdate><enddate>20220715</enddate><creator>Zhang, Xiao-Bin</creator><creator>Chen, Gong-Ping</creator><creator>Huang, Mao-Hong</creator><creator>Chen, Xiang-Xing</creator><creator>Zhan, Feng-Fu</creator><creator>He, Xiu-Zhen</creator><creator>Cai, Ling</creator><creator>Zeng, Hui-Qing</creator><general>International Scientific Literature, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20220715</creationdate><title>Bcl-2 19-kDa Interacting Protein 3 (BNIP3)-Mediated Mitophagy Attenuates Intermittent Hypoxia-Induced Human Renal Tubular Epithelial Cell Injury</title><author>Zhang, Xiao-Bin ; Chen, Gong-Ping ; Huang, Mao-Hong ; Chen, Xiang-Xing ; Zhan, Feng-Fu ; He, Xiu-Zhen ; Cai, Ling ; Zeng, Hui-Qing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-bd7ec7c41349a1c3c3f5ff1ddcd4232e2904d0edfc876267e909bec2d55aec1b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Apoptosis</topic><topic>Epithelial Cells - metabolism</topic><topic>Humans</topic><topic>Hypoxia - metabolism</topic><topic>Lab/In Vitro Research</topic><topic>Membrane Proteins - metabolism</topic><topic>Mitophagy - physiology</topic><topic>Oxygen - metabolism</topic><topic>Proto-Oncogene Proteins - metabolism</topic><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Xiao-Bin</creatorcontrib><creatorcontrib>Chen, Gong-Ping</creatorcontrib><creatorcontrib>Huang, Mao-Hong</creatorcontrib><creatorcontrib>Chen, Xiang-Xing</creatorcontrib><creatorcontrib>Zhan, Feng-Fu</creatorcontrib><creatorcontrib>He, Xiu-Zhen</creatorcontrib><creatorcontrib>Cai, Ling</creatorcontrib><creatorcontrib>Zeng, Hui-Qing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Medical science monitor</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Xiao-Bin</au><au>Chen, Gong-Ping</au><au>Huang, Mao-Hong</au><au>Chen, Xiang-Xing</au><au>Zhan, Feng-Fu</au><au>He, Xiu-Zhen</au><au>Cai, Ling</au><au>Zeng, Hui-Qing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bcl-2 19-kDa Interacting Protein 3 (BNIP3)-Mediated Mitophagy Attenuates Intermittent Hypoxia-Induced Human Renal Tubular Epithelial Cell Injury</atitle><jtitle>Medical science monitor</jtitle><addtitle>Med Sci Monit</addtitle><date>2022-07-15</date><risdate>2022</risdate><volume>28</volume><spage>e936760</spage><epage>e936760</epage><pages>e936760-e936760</pages><issn>1643-3750</issn><issn>1234-1010</issn><eissn>1643-3750</eissn><abstract>BACKGROUND As a novel pathophysiological characteristic of obstructive sleep apnea, intermittent hypoxia (IH) contributes to human renal tubular epithelial cells impairment. The underlying pathological mechanisms remain unrevealed. The present study aimed to evaluate the influence of Bcl-2 19-kDa interacting protein 3 (BNIP3)-mediated mitophagy on IH-induced renal tubular epithelial cell impairment. MATERIAL AND METHODS Human kidney proximal tubular (HK-2) cells were exposed to IH condition. IH cycles were as follows: 21% oxygen for 25 min, 21% descended to 1% for 35 min, 1% oxygen sustaining for 35 min, and 1% ascended to 21% for 25 min. The IH exposure lasted 24 h with 12 cycles of hypoxia and re-oxygenation. Both the siBNIP3 and BNIP3 vector were transfected to cells. Cell viability and apoptosis, mitochondrial morphology and function, and mitophagy were detected by cell counting kit-8, flow cytometry and TUNEL staining, transmission electron microscopy, western blotting, and immunofluorescence, respectively. RESULTS In the IH-induced HK-2 cells, inhibition of BNIP3 further aggravated mitochondrial structure damage, and decreased mitophagy level, leading to increased cell apoptosis and decreased cell viability. While overexpression of BNIP3 enhanced mitophagy, which protected mitochondrial structure, it can decrease cell death in HK-2 cells exposed to IH. CONCLUSIONS The present study showed that BNIP3-mediated mitophagy plays a protective role against IH-induced renal tubular epithelial cell impairment.</abstract><cop>United States</cop><pub>International Scientific Literature, Inc</pub><pmid>35836356</pmid><doi>10.12659/MSM.936760</doi><oa>free_for_read</oa></addata></record>
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subjects Apoptosis
Epithelial Cells - metabolism
Humans
Hypoxia - metabolism
Lab/In Vitro Research
Membrane Proteins - metabolism
Mitophagy - physiology
Oxygen - metabolism
Proto-Oncogene Proteins - metabolism
title Bcl-2 19-kDa Interacting Protein 3 (BNIP3)-Mediated Mitophagy Attenuates Intermittent Hypoxia-Induced Human Renal Tubular Epithelial Cell Injury
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