Endothelial Yes-Associated Protein 1 Promotes Astrocyte Proliferation and Maturation via Cytoplasmic Leukemia Inhibitory Factor Secretion in Oxygen-Induced Retinopathy

Ai, Liqianyu; Zhu, Jianwei; Chen, Xi; Li, Xue; Lu, Luo; Hu, Qiumei; Lin, Sen; Ye, Jian

doi:10.1167/iovs.61.4.1

Cited by 7 publications

(4 citation statements)

References 53 publications

(62 reference statements)

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“…According to the previously published method [ 21 ], rats were anesthesized, 0.9% NaCl (4℃) was used to drain the blood from the heart, then, 4% polyformaldehyde was used to fix the tissue. The eyeball was quickly removed, soaked in 4% polyformaldehyde, and fixed on ice for 2 h. The eyeball was transferred to precooled PBS, and the retina was carefully separated.…”

Section: Methodsmentioning

confidence: 99%

Axon regeneration after optic nerve injury in rats can be improved via PirB knockdown in the retina

et al. 2021

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Background In the central nervous system (CNS), three types of myelin-associated inhibitors (MAIs) exert major inhibitory effects on nerve regeneration: Nogo-A, myelin-associated glycoprotein (MAG), and oligodendrocyte-myelin glycoprotein (OMgp). MAIs have two co-receptors, Nogo receptor (NgR) and paired immunoglobulin-like receptor B (PirB). Existing studies confirm that inhibiting NgR only exerted a modest disinhibitory effect in CNS. However, the inhibitory effects of PirB on nerve regeneration after binding to MAIs are controversial too. We aimed to further investigate the effect of PirB knockdown on the neuroprotection and axonal regeneration of retinal ganglion cells (RGCs) after optic nerve injury in rats. Methods The differential expression of PirB in the retina was observed via immunofluorescence and western blotting after 1, 3, and 7 days of optic nerve injury (ONI). The retina was locally transfected with adeno-associated virus (AAV) PirB shRNA, then, the distribution of virus in tissues and cells was observed 21 days after AAV transfection to confirm the efficiency of PirB knockdown. Level of P-Stat3 and expressions of ciliary neurotrophic factor (CNTF) were detected via western blotting. RGCs were directly labeled with cholera toxin subunit B (CTB). The new axons of the optic nerve were specifically labeled with growth associated protein-43 (GAP43) via immunofluorescence. Flash visual evoked potential (FVEP) was used to detect the P1 and N1 latency, as well as N1-P1, P1-N2 amplitude to confirm visual function. Results PirB expression in the retina was significantly increased after ONI. PirB knockdown was successful and significantly promoted P-Stat3 level and CNTF expression in the retina. PirB knockdown promoted the regeneration of optic nerve axons and improved the visual function indexes such as N1-P1 and P1-N2 amplitude. Conclusions PirB is one of the key molecules that inhibit the regeneration of the optic nerve, and inhibition of PirB has an excellent effect on promoting nerve regeneration, which allows the use of PirB as a target molecule to promote functional recovery after ONI.

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Section: Methodsmentioning

confidence: 99%

Axon regeneration after optic nerve injury in rats can be improved via PirB knockdown in the retina

et al. 2021

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“…YAP was shown to be a critical regulator of angiogenic sprouting in mouse retinal vessels in a manner dependent on VE-cadherin and Ang-2, probably as a transcriptional target of YAP, and it has been suggested that disruption of VE-cadherin in ECs would activate YAP nuclear translocation and transcriptional activity [ 109 ]. In fact, the sustained binding of YAP/TAZ to the transcription factor signal transducer and activator of transcription 3 (STAT3) was shown to promote angiogenesis in a manner dependent on the increase in Ang-2 expression in ECs [ 110 , 111 ]. Moreover, the endothelial YAP deletion reduced the LIF secretion, caused a disruption of the astrocytic network, and reduced the astrocyte differentiation.…”

Section: Feedback Between Astrocytes and Blood Vesselsmentioning

confidence: 99%

“…Moreover, the endothelial YAP deletion reduced the LIF secretion, caused a disruption of the astrocytic network, and reduced the astrocyte differentiation. In addition, in astrocyte cultures treated with conditioned medium from ECs that overexpressed YAP, increased astrocyte differentiation was observed [ 111 ]. This finding suggests that YAP regulates the LIF secretion from ECs that promote the maturation of astrocytic networks.…”

Section: Feedback Between Astrocytes and Blood Vesselsmentioning

confidence: 99%

Key Role of Astrocytes in Postnatal Brain and Retinal Angiogenesis

Puebla

Tapía

Espinoza³

2022

IJMS

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Angiogenesis is a key process in various physiological and pathological conditions in the nervous system and in the retina during postnatal life. Although an increasing number of studies have addressed the role of endothelial cells in this event, the astrocytes contribution in angiogenesis has received less attention. This review is focused on the role of astrocytes as a scaffold and in the stabilization of the new blood vessels, through different molecules release, which can modulate the angiogenesis process in the brain and in the retina. Further, differences in the astrocytes phenotype are addressed in glioblastoma, one of the most devastating types of brain cancer, in order to provide potential targets involved in the cross signaling between endothelial cells, astrocytes and glioma cells, that mediate tumor progression and pathological angiogenesis. Given the relevance of astrocytes in angiogenesis in physiological and pathological conditions, future studies are required to better understand the interrelation between endothelial and astrocyte signaling pathways during this process.

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“…In addition, recent findings on Yap haploinsufficiency indicate Müller glia dysfunction, late-onset cone degeneration, and reduced cone-mediated visual response [ 57 ]. Finally, YAP deficient endothelial cells show damaged retinal vascularisation and obstructive astrocyte network formation and maturation [ 58 ].…”

Section: Yap and Actin Cytoskeleton In Eye Development And Diseasementioning

confidence: 99%

The Molecular Network of YAP/Yorkie at the Cell Cortex and their Role in Ocular Morphogenesis

Skouloudaki

Papadopoulos

Hurd

2020

IJMS

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During development, the precise control of tissue morphogenesis requires changes in the cell number, size, shape, position, and gene expression, which are driven by both chemical and mechanical cues from the surrounding microenvironment. Such physical and architectural features inform cells about their proliferative and migratory capacity, enabling the formation and maintenance of complex tissue architecture. In polarised epithelia, the apical cell cortex, a thin actomyosin network that lies directly underneath the apical plasma membrane, functions as a platform to facilitate signal transmission between the external environment and downstream signalling pathways. One such signalling pathway culminates in the regulation of YES-associated protein (YAP) and TAZ transcriptional co-activators and their sole Drosophila homolog, Yorkie, to drive proliferation and differentiation. Recent studies have demonstrated that YAP/Yorkie exhibit a distinct function at the apical cell cortex. Here, we review recent efforts to understand the mechanisms that regulate YAP/Yki at the apical cell cortex of epithelial cells and how normal and disturbed YAP–actomyosin networks are involved in eye development and disease.

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Endothelial Yes-Associated Protein 1 Promotes Astrocyte Proliferation and Maturation via Cytoplasmic Leukemia Inhibitory Factor Secretion in Oxygen-Induced Retinopathy

Cited by 7 publications

References 53 publications

Axon regeneration after optic nerve injury in rats can be improved via PirB knockdown in the retina

Axon regeneration after optic nerve injury in rats can be improved via PirB knockdown in the retina

Key Role of Astrocytes in Postnatal Brain and Retinal Angiogenesis

The Molecular Network of YAP/Yorkie at the Cell Cortex and their Role in Ocular Morphogenesis

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