Stanniocalcin 1a is a Ca2+-regulated switch controlling epithelial cell quiescence-proliferation balance and Ca2+uptake DOI Creative Commons
Shuang Li, Chengdong Liu, Allison Goldstein

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2020, Volume and Issue: unknown

Published: Sept. 10, 2020

Abstract The mechanisms governing cell quiescence-proliferation balance are poorly defined. Using a zebrafish model, here we report that Stc1a, glycoprotein known as hypocalcemic hormone, not only inhibits epithelial calcium uptake but also functions Ca 2+ -regulated switch controlling balance. Among the 4 stc genes, stc1a expression is [Ca ]-dependent. Genetic deletion of , stc2b resulted in elevated body contents, ectopic deposit, swelling, and premature death. Reducing channel Trpv6-mediated alleviated these phenotypes. Loss Stc1a promoted quiescent cells to re-enter cycle. This action was accompanied by local IGF signaling activation increased papp-aa zinc metalloproteinase degrading Igfbp5a. or igfbp5a abolished reactivation -/- mutants. Likewise, inhibition IGF1 receptor, PI3 kinase, Akt, Tor reactivation. These results reveal plays dual roles regulating implicate Trpv6 Papp-aa-Igfbp5a-IGF functions.

Language: Английский

Cell surface thermal proteome profiling tracks perturbations and drug targets on the plasma membrane DOI
Mathias Kalxdorf,

Ina Günthner,

Isabelle Becher

et al.

Nature Methods, Journal Year: 2021, Volume and Issue: 18(1), P. 84 - 91

Published: Jan. 1, 2021

Language: Английский

Citations

74
Neurological and metabolic related pathophysiologies and treatment of comorbid diabetes with depression DOI Creative Commons

Sixin Li,

Dong Yang, Chao Zhou

et al.

CNS Neuroscience & Therapeutics, Journal Year: 2023, Volume and Issue: 30(4)

Published: Nov. 6, 2023

Abstract Background The comorbidity between diabetes mellitus and depression was revealed, increased the prevalence of depressive disorder, which ranked 13th in leading causes disability‐adjusted life‐years. Insulin resistance, is common mellitus, has risk symptoms both humans animals. However, mechanisms behind are multi‐factorial complicated. There still no causal chain to explain exactly. Moreover, Selective serotonin reuptake inhibitors, insulin metformin, recommended for treating mellitus‐induced depression, were found be a factor some complications diabetes. Aims Given these problems, many researchers made remarkable efforts analyze complicating from different aspects, including stress Hypothalamic–Pituitary–Adrenal axis, neurological system, oxidative stress, inflammation. Drug therapy, such as Hydrogen Sulfide, Cannabidiol, Ascorbic Acid Hesperidin, conducive alleviating depression. Here, we reviewed exact pathophysiology underlying disorder drug therapy. Methods review refers available literature PubMed Web Science, searching critical terms related Results In this review, that brain structure function, neurogenesis, brain‐derived neurotrophic glucose lipid metabolism involved comorbidity. Obesity might lead through reduced adiponectin leptin resistin. addition, therapy displayed could expand region potential Conclusions summarizes It also overviews with anti‐diabetic anti‐depressant effects.

Language: Английский

Citations

26
Potential role of insulin on the pathogenesis of depression DOI Creative Commons

Xiao Han Zou,

Li Sun, Wei Yang

et al.

Cell Proliferation, Journal Year: 2020, Volume and Issue: 53(5)

Published: April 13, 2020

Abstract The regulation of insulin on depression and depression‐like behaviour has been widely reported. Insulin activation its receptor can promote learning memory, affect the hypothalamic‐pituitary‐adrenal axis (HPA) balance, regulate secretion neurotrophic factors neurotransmitters, interact with gastrointestinal microbiome, exert neuroprotective effects have an impact depression. However, role remains largely unclear. Therefore, in this review, we summarized potential It may provide new insight for clarifying pathogenesis

Language: Английский

Citations

56
STRIPAK Members Orchestrate Hippo and Insulin Receptor Signaling to Promote Neural Stem Cell Reactivation DOI Creative Commons
Jon Gil-Ranedo,

Eleanor Gonzaga,

Karolina Jaworek

et al.

Cell Reports, Journal Year: 2019, Volume and Issue: 27(10), P. 2921 - 2933.e5

Published: June 1, 2019

Adult stem cells reactivate from quiescence to maintain tissue homeostasis and in response injury. How the underlying regulatory signals are integrated is largely unknown. Drosophila neural (NSCs) also leave generate adult neurons glia, a process that dependent on Hippo signaling inhibition activation of insulin-like receptor (InR)/PI3K/Akt cascade. We performed transcriptome analysis individual quiescent reactivating NSCs harvested directly brains identified conserved STRIPAK complex members mob4, cka, PP2A (microtubule star, mts). show PP2A/Mts phosphatase, with its subunit Widerborst, maintains NSC quiescence, preventing premature InR/PI3K/Akt signaling. Conversely, an increase Mob4 Cka levels promotes reactivation. essential recruit into kinase, resulting pathway inhibition. propose Mob4/Cka/Mts functions as intrinsic molecular switch coordinating pathways enabling

Language: Английский

Citations

52
Waking up quiescent neural stem cells: Molecular mechanisms and implications in neurodevelopmental disorders DOI Creative Commons
Wei Ding, Jiawen Huang, Hongyan Wang

et al.

PLoS Genetics, Journal Year: 2020, Volume and Issue: 16(4), P. e1008653 - e1008653

Published: April 23, 2020

Neural stem cells (NSCs) are crucial for development, regeneration, and repair of the nervous system. Most NSCs in mammalian adult brains quiescent, but response to extrinsic stimuli, they can exit from quiescence become reactivated give rise new neurons. The delicate balance between NSC activation is important neurogenesis maintenance. However, how transit remains largely elusive. Here, we discuss our current understanding molecular mechanisms underlying reactivation quiescent NSCs. We review recent advances on signaling pathways originated niche their crosstalk regulating reactivation. also highlight intrinsic paradigms that control Drosophila systems. emerging evidence modeling human neurodevelopmental disorders using

Language: Английский

Citations

46
Neural Stem Cell Activation and the Role of Protein Synthesis DOI Open Access

Avni Baser,

Maxim A. Skabkin,

Ana Martin‐Villalba

et al.

Brain Plasticity, Journal Year: 2017, Volume and Issue: 3(1), P. 27 - 41

Published: Jan. 10, 2017

Adult neural stem cells are generated at embryonic stages by entering a quiescent state that allows their retention into adulthood and thereby maintenance of life-long brain homeostasis.Thus, tight balance between the quiescence activation is instrumental to meet demands for specific cell type correct numbers, given time position.Protein synthesis most energy-consuming process within and, not surprisingly, it occurs low rates in cells.This way adjust energy constraints avoid premature depletion.Stem characterized upregulation protein followed division differentiation.The role such as causative or rather consequence remains elusive.Here we summarize recent findings connecting regulation synthesis, particularly focusing on adult ventricular zone.

Language: Английский

Citations

36
Golgi-dependent reactivation and regeneration of Drosophila quiescent neural stem cells DOI Creative Commons
Mahekta R. Gujar, Yang Gao, Xiang Teng

et al.

Developmental Cell, Journal Year: 2023, Volume and Issue: 58(19), P. 1933 - 1949.e5

Published: Aug. 10, 2023

The ability of stem cells to switch between quiescent and proliferative states is crucial for maintaining tissue homeostasis regeneration. In Drosophila, neural (qNSCs) extend a primary protrusion, hallmark qNSCs. Here, we have found that qNSC protrusions can be regenerated upon injury. This regeneration process relies on the Golgi apparatus acts as major acentrosomal microtubule-organizing center in A Golgi-resident GTPase Arf1 its guanine nucleotide exchange factor Sec71 promote NSC reactivation via regulation microtubule growth. physically associates with new effector mini spindles (Msps)/XMAP215, polymerase. Finally, functions upstream Msps target cell adhesion molecule E-cadherin NSC-neuropil contact sites during reactivation. Our findings established Drosophila qNSCs model identified Arf1/Sec71-Msps pathway growth

Language: Английский

Citations

10
The Critical Balance Between Quiescence and Reactivation of Neural Stem Cells DOI Creative Commons
Adam M. Elkin, Sarah Robbins, Claudia S. Barros

et al.

Biomolecules, Journal Year: 2025, Volume and Issue: 15(5), P. 672 - 672

Published: May 6, 2025

Neural stem cells (NSC) are multipotent, self-renewing that give rise to all neural cell types within the central nervous system. During adulthood, most NSCs exist in a quiescent state which can be reactivated response metabolic and signalling changes, allowing for long-term continuous neurogenesis injury. Ensuring critical balance between quiescence reactivation is required maintain limited NSC reservoir replenishment throughout lifetime. The precise mechanisms pathways behind this at focus of current research. In review, we highlight discuss recent studies using Drosophila, mammalian zebrafish models contributing understanding molecular underlying NSCs.

Language: Английский

Citations

0
Histone lysine methyltransferase Pr‐set7/SETD8 promotes neural stem cell reactivation DOI Creative Commons
Jiawen Huang, Mahekta R. Gujar, Qiannan Deng

et al.

EMBO Reports, Journal Year: 2021, Volume and Issue: 22(4)

Published: Feb. 10, 2021

The ability of neural stem cells (NSCs) to switch between quiescence and proliferation is crucial for brain development homeostasis. Increasing evidence suggests that variants histone lysine methyltransferases including KMT5A are associated with neurodevelopmental disorders. However, the function KMT5A/Pr-set7/SETD8 in central nervous system not well established. Here, we show Drosophila Pr-Set7 a novel regulator NSC reactivation. Loss pr-set7 causes delay reactivation loss H4K20 monomethylation brain. Through NSC-specific vivo profiling, demonstrate Pr-set7 binds promoter region cyclin-dependent kinase 1 (cdk1) Wnt pathway transcriptional co-activator earthbound1/jerky (ebd1). Further validation indicates required expression cdk1 ebd1 Similar Pr-set7, Cdk1 Ebd1 promote Finally, overexpression significantly suppressed defects observed pr-set7-depleted brains. Therefore, promotes by regulating signaling cell cycle progression. Our findings may contribute understanding mammalian KMT5A/PR-SET7/SETD8 during development.

Language: Английский

Citations

21
Astrocytes control quiescent NSC reactivation via GPCR signaling–mediated F-actin remodeling DOI Creative Commons
Kun‐Yang Lin, Mahekta R. Gujar, Jiaen Lin

et al.

Science Advances, Journal Year: 2024, Volume and Issue: 10(30)

Published: July 24, 2024

The transitioning of neural stem cells (NSCs) between quiescent and proliferative states is fundamental for brain development homeostasis. Defects in NSC reactivation are associated with neurodevelopmental disorders.

Language: Английский

Citations

3