Vitamin D Receptor Regulates Autophagy to Inhibit Apoptosis and Promote Proliferation in Hepatocyte Injury
BACKGROUND: Oxidative stress is an important mechanism in liver ischemia/reperfusion (I/R) injury. Hepatocyte apoptosis and proliferation occur in parallel with liver I/R injury, and the degree of apoptosis and proliferation determines the effects on hepatocytes. Vitamin D receptor (VDR) can lessen liver I/R injury, but previous studies focused mostly on inflammation and immunity.
METHODS: H2O2 was used to induce hepatocyte injury. Before treatment with H2O2, Hep-3B cells were pretreated with paricalcitol (PC) and siRNA-VDR. Rapamycin and chloroquine were also applied in the study.
RESULTS: The number of apoptotic cells was measured with an annexin V (AV) -fluorescein isothiocyanate apoptosis detection kit. Expression of proteins was measured by western blotting. As compared with the H2O2+Hep-3B group, levels of AV/PI, cleaved caspase-3, and p62 were lower, and expression levels of Bcl-2, proliferating cell nuclear antigen, and VDR were higher, in the PC+H2O2+Hep-3B group. When the VDR gene was silenced by siRNA-VDR in the siRNA-VDR+H2O2+Hep-3B group, expressions of AV/PI, cleaved caspase-3, and p62 were upregulated, and expressions of Bcl-2, proliferating cell nuclear antigen, and VDR were downregulated, as compared with values for the siRNA-NC+H2O2+Hep-3B group. Treatment with rapamycin or chloroquine partially reversed the effect of PC and siRNA-VDR on apoptosis and proliferation.
CONCLUSIONS: VDR mediates hepatocyte apoptosis and proliferation through autophagy.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2023 |
|---|---|
| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:90 |
|---|---|
| Enthalten in: |
Journal of Nippon Medical School = Nippon Ika Daigaku zasshi - 90(2023), 1 vom: 28., Seite 89-95 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Fang, Mingming [VerfasserIn] |
|---|
| Links: |
|---|
| Anmerkungen: |
Date Completed 20.03.2023 Date Revised 20.03.2023 published: Print Citation Status MEDLINE |
|---|
| doi: |
10.1272/jnms.JNMS.2023_90-114 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM35413745X |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM35413745X | ||
| 003 | DE-627 | ||
| 005 | 20231226061556.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231226s2023 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1272/jnms.JNMS.2023_90-114 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1180.xml |
| 035 | |a (DE-627)NLM35413745X | ||
| 035 | |a (NLM)36908130 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Fang, Mingming |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Vitamin D Receptor Regulates Autophagy to Inhibit Apoptosis and Promote Proliferation in Hepatocyte Injury |
| 264 | 1 | |c 2023 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 20.03.2023 | ||
| 500 | |a Date Revised 20.03.2023 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a BACKGROUND: Oxidative stress is an important mechanism in liver ischemia/reperfusion (I/R) injury. Hepatocyte apoptosis and proliferation occur in parallel with liver I/R injury, and the degree of apoptosis and proliferation determines the effects on hepatocytes. Vitamin D receptor (VDR) can lessen liver I/R injury, but previous studies focused mostly on inflammation and immunity | ||
| 520 | |a METHODS: H2O2 was used to induce hepatocyte injury. Before treatment with H2O2, Hep-3B cells were pretreated with paricalcitol (PC) and siRNA-VDR. Rapamycin and chloroquine were also applied in the study | ||
| 520 | |a RESULTS: The number of apoptotic cells was measured with an annexin V (AV) -fluorescein isothiocyanate apoptosis detection kit. Expression of proteins was measured by western blotting. As compared with the H2O2+Hep-3B group, levels of AV/PI, cleaved caspase-3, and p62 were lower, and expression levels of Bcl-2, proliferating cell nuclear antigen, and VDR were higher, in the PC+H2O2+Hep-3B group. When the VDR gene was silenced by siRNA-VDR in the siRNA-VDR+H2O2+Hep-3B group, expressions of AV/PI, cleaved caspase-3, and p62 were upregulated, and expressions of Bcl-2, proliferating cell nuclear antigen, and VDR were downregulated, as compared with values for the siRNA-NC+H2O2+Hep-3B group. Treatment with rapamycin or chloroquine partially reversed the effect of PC and siRNA-VDR on apoptosis and proliferation | ||
| 520 | |a CONCLUSIONS: VDR mediates hepatocyte apoptosis and proliferation through autophagy | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a apoptosis | |
| 650 | 4 | |a autophagy | |
| 650 | 4 | |a hepatocyte injury | |
| 650 | 4 | |a proliferation | |
| 650 | 4 | |a vitamin D receptor | |
| 650 | 7 | |a Caspase 3 |2 NLM | |
| 650 | 7 | |a EC 3.4.22.- |2 NLM | |
| 650 | 7 | |a Chloroquine |2 NLM | |
| 650 | 7 | |a 886U3H6UFF |2 NLM | |
| 650 | 7 | |a Hydrogen Peroxide |2 NLM | |
| 650 | 7 | |a BBX060AN9V |2 NLM | |
| 650 | 7 | |a Proliferating Cell Nuclear Antigen |2 NLM | |
| 650 | 7 | |a Proto-Oncogene Proteins c-bcl-2 |2 NLM | |
| 650 | 7 | |a Receptors, Calcitriol |2 NLM | |
| 650 | 7 | |a RNA, Small Interfering |2 NLM | |
| 650 | 7 | |a Sirolimus |2 NLM | |
| 650 | 7 | |a W36ZG6FT64 |2 NLM | |
| 650 | 7 | |a VDR protein, human |2 NLM | |
| 700 | 1 | |a Zhong, Chen |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Journal of Nippon Medical School = Nippon Ika Daigaku zasshi |d 2000 |g 90(2023), 1 vom: 28., Seite 89-95 |w (DE-627)NLM106816829 |x 1347-3409 |7 nnns |
| 773 | 1 | 8 | |g volume:90 |g year:2023 |g number:1 |g day:28 |g pages:89-95 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1272/jnms.JNMS.2023_90-114 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 90 |j 2023 |e 1 |b 28 |h 89-95 | ||