Overexpression of LINC00672 promotes autophagy in Alzheimer's disease by upregulating GPNMB.
<h4>Background</h4>Alzheimer's disease (AD) is an irreversible neurodegenerative brain disorder, and autophagy crafts a new dawn on AD therapeutics. However, whether LINC00672 exerts its biological effects involvement in autophagy-mediated mechanisms in AD remain obscure.<h4>M...
Saved in:
| Main Authors: | , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2025-01-01
|
| Series: | PLoS ONE |
| Online Access: | https://doi.org/10.1371/journal.pone.0322708 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1850265840140681216 |
|---|---|
| author | Lingyi Gao Shijun Hu Yan Lv Guoxian Zheng Zhichuan Lin |
| author_facet | Lingyi Gao Shijun Hu Yan Lv Guoxian Zheng Zhichuan Lin |
| author_sort | Lingyi Gao |
| collection | DOAJ |
| description | <h4>Background</h4>Alzheimer's disease (AD) is an irreversible neurodegenerative brain disorder, and autophagy crafts a new dawn on AD therapeutics. However, whether LINC00672 exerts its biological effects involvement in autophagy-mediated mechanisms in AD remain obscure.<h4>Methods</h4>SH-SY5Y cells were treated with Amyloid Beta 1-42 (Aβ1-42, Aβ), while an AD mouse model was established using streptozotocin (STZ). The effects of LINC00672 overexpression on cell proliferation, apoptosis, and autophagy were evaluated in Aβ-stimulated SH-SY5Y cells. Besides, the impact of LINC00672 on cognitive function and pathological changes of the hippocampal tissues were validated in AD mice. Additionally, the interaction between LINC00672 overexpression and GPNMB silencing were determined in vitro.<h4>Results</h4>Aβ stimulation diminished viability, augmented apoptosis, restricted the activation of autophagy in SH-SY5Y cells, while these alterations were partially abolished by LINC00672 overexpression. Furthermore, LINC00672 upregulation could improve cognitive impairment, and attenuate neuronal damage and even death in the STZ-treated AD mice. Additionally, GPNMB knockdown aggravated the improved neuronal injury and relatively restrained autophagy in Aβ-stimulated cells after LINC00672 overexpression.<h4>Conclusions</h4>LINC00672 exerted a protective effect in the AD progression by upregulating GPNMB to promote autophagy. |
| format | Article |
| id | doaj-art-0ed6ea50af0641d1934471fa65fb1957 |
| institution | OA Journals |
| issn | 1932-6203 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj-art-0ed6ea50af0641d1934471fa65fb19572025-08-20T01:54:19ZengPublic Library of Science (PLoS)PLoS ONE1932-62032025-01-01205e032270810.1371/journal.pone.0322708Overexpression of LINC00672 promotes autophagy in Alzheimer's disease by upregulating GPNMB.Lingyi GaoShijun HuYan LvGuoxian ZhengZhichuan Lin<h4>Background</h4>Alzheimer's disease (AD) is an irreversible neurodegenerative brain disorder, and autophagy crafts a new dawn on AD therapeutics. However, whether LINC00672 exerts its biological effects involvement in autophagy-mediated mechanisms in AD remain obscure.<h4>Methods</h4>SH-SY5Y cells were treated with Amyloid Beta 1-42 (Aβ1-42, Aβ), while an AD mouse model was established using streptozotocin (STZ). The effects of LINC00672 overexpression on cell proliferation, apoptosis, and autophagy were evaluated in Aβ-stimulated SH-SY5Y cells. Besides, the impact of LINC00672 on cognitive function and pathological changes of the hippocampal tissues were validated in AD mice. Additionally, the interaction between LINC00672 overexpression and GPNMB silencing were determined in vitro.<h4>Results</h4>Aβ stimulation diminished viability, augmented apoptosis, restricted the activation of autophagy in SH-SY5Y cells, while these alterations were partially abolished by LINC00672 overexpression. Furthermore, LINC00672 upregulation could improve cognitive impairment, and attenuate neuronal damage and even death in the STZ-treated AD mice. Additionally, GPNMB knockdown aggravated the improved neuronal injury and relatively restrained autophagy in Aβ-stimulated cells after LINC00672 overexpression.<h4>Conclusions</h4>LINC00672 exerted a protective effect in the AD progression by upregulating GPNMB to promote autophagy.https://doi.org/10.1371/journal.pone.0322708 |
| spellingShingle | Lingyi Gao Shijun Hu Yan Lv Guoxian Zheng Zhichuan Lin Overexpression of LINC00672 promotes autophagy in Alzheimer's disease by upregulating GPNMB. PLoS ONE |
| title | Overexpression of LINC00672 promotes autophagy in Alzheimer's disease by upregulating GPNMB. |
| title_full | Overexpression of LINC00672 promotes autophagy in Alzheimer's disease by upregulating GPNMB. |
| title_fullStr | Overexpression of LINC00672 promotes autophagy in Alzheimer's disease by upregulating GPNMB. |
| title_full_unstemmed | Overexpression of LINC00672 promotes autophagy in Alzheimer's disease by upregulating GPNMB. |
| title_short | Overexpression of LINC00672 promotes autophagy in Alzheimer's disease by upregulating GPNMB. |
| title_sort | overexpression of linc00672 promotes autophagy in alzheimer s disease by upregulating gpnmb |
| url | https://doi.org/10.1371/journal.pone.0322708 |
| work_keys_str_mv | AT lingyigao overexpressionoflinc00672promotesautophagyinalzheimersdiseasebyupregulatinggpnmb AT shijunhu overexpressionoflinc00672promotesautophagyinalzheimersdiseasebyupregulatinggpnmb AT yanlv overexpressionoflinc00672promotesautophagyinalzheimersdiseasebyupregulatinggpnmb AT guoxianzheng overexpressionoflinc00672promotesautophagyinalzheimersdiseasebyupregulatinggpnmb AT zhichuanlin overexpressionoflinc00672promotesautophagyinalzheimersdiseasebyupregulatinggpnmb |