LINC00173 regulates polycystic ovarian syndrome progression by promoting apoptosis and repressing proliferation in ovarian granulosa cells via the microRNA-124-3p (miR-124-3p)/jagged canonical Notch ligand 1 (JAG1) pathway DOI Open Access
Lan Chen, Caixia Kong

Bioengineered, Journal Year: 2022, Volume and Issue: 13(4), P. 10373 - 10385

Published: April 1, 2022

As an endocrine and metabolic disorder, polycystic ovarian syndrome (PCOS) is common in females at childbearing age. Our work was intended to uncover the underlying role of LINC00173 its potential regulatory mechanism PCOS based on two cell lines (PCOS granulosa cells KGN cells) vivo model established from Sprague Dawley rats. It revealed that JAG1 expressions were upregulated, while miR-124-3p poorly expressed patients Functional assays showed overexpression repressed proliferation stimulated apoptosis cells, downregulation exhibited opposite effects. Besides, it verified upregulated expression via competitively binding miR-124-3p. Similarly, abundance inversely related level PCOS. Subsequently, rescue elucidated upregulation or eliminated effects mediated by knockdown. In addition, found adversely modulated positively LINC00173. Moreover, further demonstrated reduced vitality increased induced overexpressing could be relieved deletion. These findings suggested a latent regulating factor for progression modulating miR-124-3p/JAG1 cascade.

Language: Английский

Dexmedetomidine Alleviates Hypoxia-Induced Synaptic Loss and Cognitive Impairment via Inhibition of Microglial NOX2 Activation in the Hippocampus of Neonatal Rats DOI Creative Commons
Xiaohui Chen, Dongtai Chen, Qiang Li

et al.

Oxidative Medicine and Cellular Longevity, Journal Year: 2021, Volume and Issue: 2021(1)

Published: Jan. 1, 2021

Background . Perinatal hypoxia is a universal cause of death and neurological deficits in neonates worldwide. Activation microglial NADPH oxidase 2 (NOX2) leads to oxidative stress neuroinflammation, which may contribute hypoxic damage the developing brain. Dexmedetomidine has been reported exert potent neuroprotection several diseases, but mechanism remains unclear. We investigated whether dexmedetomidine acts through NOX2 reduce neonatal brain damage. Methods The potential role dexmedetomidine‐mediated alleviation was evaluated cultured BV2 microglia rats subjected hypoxia. In vivo , received (25 μ g/kg, i.p.) 30 min before or immediately after (5% O h). Apocynin‐mediated NOX inhibition lentivirus‐mediated overexpression were applied further assess involvement activation. Results Pre‐ posttreatment with alleviated hypoxia‐induced cognitive impairment, restored damaged synapses, increased postsynaptic density‐95 synaptophysin protein expression following Importantly, treatment suppressed activation subsequent neuroinflammatory response, as reflected by reduced 4‐hydroxynonenal ROS accumulation, decreased nuclear NF‐ κ B p65 proinflammatory cytokine levels hippocampus. addition, treating primary hippocampal neurons conditioned medium (CM) from hypoxia‐activated resulted neuronal damage, CM dexmedetomidine‐treated microglia. Moreover, neuroprotective effect reversed NOX2‐overexpressing diminished apocynin‐pretreated rats. Conclusion targets neuroinflammation subsequently protects against synaptic loss

Language: Английский

Citations

30
MicroRNAs: protective regulators for neuron growth and development DOI Creative Commons
Zhongdao Wu, Ying Feng,

Zhi-Xuan Ma

et al.

Neural Regeneration Research, Journal Year: 2022, Volume and Issue: 18(4), P. 734 - 734

Published: Sept. 21, 2022

MicroRNAs (miRNAs) play an important regulatory role in neuronal growth and development. Different miRNAs target different genes to protect neurons ways, such as by avoiding apoptosis, preventing degeneration mediated conditional mediators, loss, weakening certain neurotoxic mechanisms, damage neurons, reducing inflammatory them. The high expression of the brain has significantly facilitated their development protective targets for therapy, including neuroprotection recovery. miRNA is indispensable turn, beneficial checking progression various diseases nervous system. It can thus be used therapeutic models diseases. This review provides introduction effects on case or models, then reference values reflections relevant treatments benefit future research area.

Language: Английский

Citations

22
Dexmedetomidine alleviates sevoflurane-induced neurotoxicity during late pregnancy by modulating apoptotic pathways and BDNF receptor expression DOI
Zhiqiang Yu, Qi Zhao,

Fengxia Duan

et al.

Experimental Brain Research, Journal Year: 2025, Volume and Issue: 243(4)

Published: March 21, 2025

Language: Английский

Citations

0
Regulation of Apoptotic Pathways by MicroRNAs: A Therapeutic Strategy for Alzheimer’s Disease DOI
Mohamed J. Saadh,

Faris Anad Muhammad,

Tuqa S. Alazzawi

et al.

Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown

Published: April 12, 2025

Language: Английский

Citations

0
LINC00173 regulates polycystic ovarian syndrome progression by promoting apoptosis and repressing proliferation in ovarian granulosa cells via the microRNA-124-3p (miR-124-3p)/jagged canonical Notch ligand 1 (JAG1) pathway DOI Open Access
Lan Chen, Caixia Kong

Bioengineered, Journal Year: 2022, Volume and Issue: 13(4), P. 10373 - 10385

Published: April 1, 2022

As an endocrine and metabolic disorder, polycystic ovarian syndrome (PCOS) is common in females at childbearing age. Our work was intended to uncover the underlying role of LINC00173 its potential regulatory mechanism PCOS based on two cell lines (PCOS granulosa cells KGN cells) vivo model established from Sprague Dawley rats. It revealed that JAG1 expressions were upregulated, while miR-124-3p poorly expressed patients Functional assays showed overexpression repressed proliferation stimulated apoptosis cells, downregulation exhibited opposite effects. Besides, it verified upregulated expression via competitively binding miR-124-3p. Similarly, abundance inversely related level PCOS. Subsequently, rescue elucidated upregulation or eliminated effects mediated by knockdown. In addition, found adversely modulated positively LINC00173. Moreover, further demonstrated reduced vitality increased induced overexpressing could be relieved deletion. These findings suggested a latent regulating factor for progression modulating miR-124-3p/JAG1 cascade.

Language: Английский

Citations

16