Participation of cAMP/PKA-Mediated Signaling Pathways in Functional Activity of Regeneration-Competent Cells in the Nervous Tissue under Conditions of Ethanol-Induced Neurodegeneration

Zyuz’kov, G. N.; Мирошниченко, Л. А.; Polyakova, T. Yu.; Ставрова, Л. А.; Симанина, Е. В.; Агафонов, В. И.; Жданов, В. В.

doi:10.1007/s10517-019-04608-8

Cited by 3 publications

(2 citation statements)

References 10 publications

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“…Cx43-formed GJs in stem cell-niche junctions also regulate stem cell functions in hematopoietic and nervous systems, but the GJ-transmitted signals are still missing ( 46 ). cAMP-PKA signaling is known to regulate hematopoietic stem cells ( 49 ) and neural stem cells ( 50 ). These raise the interesting possibility that the GJ-transported cAMP from the niche also regulates stem cell functions.…”

Section: Discussionmentioning

confidence: 99%

Gap junction–transported cAMP from the niche controls stem cell progeny differentiation

Tu,

Tang,

et al. 2023

Proc. Natl. Acad. Sci. U.S.A.

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The niche has been shown to control stem cell self-renewal in different tissue types and organisms. Recently, a separate niche has been proposed to control stem cell progeny differentiation, called the differentiation niche. However, it remains poorly understood whether and how the differentiation niche directly signals to stem cell progeny to control their differentiation. In the Drosophila ovary, inner germarial sheath (IGS) cells contribute to two separate niche compartments for controlling both germline stem cell (GSC) self-renewal and progeny differentiation. In this study, we show that IGS cells express Inx2 protein, which forms gap junctions (GJs) with germline-specific Zpg protein to control stepwise GSC lineage development, including GSC self-renewal, germline cyst formation, meiotic double-strand DNA break formation, and oocyte specification. Germline-specific Zpg and IGS-specific Inx2 knockdowns cause similar defects in stepwise GSC development. Additionally, secondary messenger cAMP is transported from IGS cells to GSCs and their progeny via GJs to activate PKA signaling for controlling stepwise GSC development. Therefore, this study demonstrates that the niche directly controls GSC progeny differentiation via the GJ-cAMP-PKA signaling axis, which provides important insights into niche control of stem cell differentiation and highlights the importance of GJ-transported cAMP in tissue regeneration. This may represent a general strategy for the niche to control adult stem cell development in various tissue types and organisms since GJs and cAMP are widely distributed.

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Section: Discussionmentioning

confidence: 99%

Gap junction–transported cAMP from the niche controls stem cell progeny differentiation

Tu,

Tang,

et al. 2023

Proc. Natl. Acad. Sci. U.S.A.

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“…The cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) signaling pathway plays an important role in controlling the proliferation and differentiation of progenitor cells and the production of cytokines ( 18 ). It has been revealed that PKA phosphorylation is associated with CNS injury in vivo and in vitro ( 19 ).…”

Section: Introductionmentioning

confidence: 99%

Melatonin alleviates traumatic brain injury‑induced anxiety‑like behaviors in rats: Roles of the protein kinase A/cAMP‑response element binding signaling pathway

Xie

Fan

et al. 2022

Exp Ther Med

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Melatonin is a hormone produced by the pineal gland. Given its capabilities of neuroprotection and low neurotoxicity, melatonin could be a therapeutic strategy for traumatic brain injury (TBI). The present study was conducted to determine the neuroprotective effects of melatonin on TBI-induced anxiety and the possible molecular mechanism. Rats were randomly divided into seven groups. The rodent model of TBI was established using the weight-drop method. Melatonin was administered by intraperitoneal injection at a dose of 10 mg/kg after TBI. H89 (0.02 mg/kg), a special protein kinase A (PKA) inhibitor, or dibutyryl-cyclic adenosine monophosphate (cAMP; 0.1 mg/kg), an activator of PKA, were administered by stereotactic injection of the brain to evaluate the roles of PKA and cAMP-response element-binding protein (CREB) in melatonin-related mood regulation, respectively. At 30 days post-TBI, the changes in anxiety-like behaviors in rats were measured using the open field and elevated plus maze tests. At 24 h post-TBI, the number of activated astrocytes and neuronal apoptosis were evaluated using immunofluorescence assay. The expression levels of inflammatory cytokines (TNF-α and IL-6) in the amygdala were measured using an enzyme-linked immunosorbent assay. The expression levels of PKA, phosphorylated (p)-PKA, CREB, p-CREB, NF-κB and p-NF-κB in the amygdala were detected using western blotting. It was revealed that melatonin partially reversed TBI-induced anxiety-like behavior in rats, and decreased the number of activated astrocytes and neuronal apoptosis in the amygdala induced by TBI. H89 partially blocked the neuroprotective effects of melatonin; while dibutyryl-cAMP not only reduced the H89-induced emotional disturbance but also enhanced the protective effects of melatonin against TBI. Overall, melatonin can alleviate TBI-induced anxiety-like behaviors in rats. Moreover, the underlying mechanism may be associated with the activation of the PKA/CREB signaling pathway.

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Role of MAPK ERK1/2 and p38 in the Regulation of Secretory Functions of Different Populations of Neuroglia in Ethanol-Induced Neurodegeneration

et al. 2021

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Participation of cAMP/PKA-Mediated Signaling Pathways in Functional Activity of Regeneration-Competent Cells in the Nervous Tissue under Conditions of Ethanol-Induced Neurodegeneration

Cited by 3 publications

References 10 publications

Gap junction–transported cAMP from the niche controls stem cell progeny differentiation

Gap junction–transported cAMP from the niche controls stem cell progeny differentiation

Melatonin alleviates traumatic brain injury‑induced anxiety‑like behaviors in rats: Roles of the protein kinase A/cAMP‑response element binding signaling pathway

Role of MAPK ERK1/2 and p38 in the Regulation of Secretory Functions of Different Populations of Neuroglia in Ethanol-Induced Neurodegeneration

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