Ghrelin Regulates Expression of the Transcription Factor Pax6 in Hypoxic Brain Progenitor Cells and Neurons

Stoyanova, Irina; Klymenko, Andrii; Willms, Jeannette; Döppner, Thorsten R.; Tonchev, Anton B.; Lutz, David

doi:10.3390/cells11050782

Cited by 5 publications

(4 citation statements)

References 105 publications

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“…Similar to our results, HIF1α expression was enhanced in the BCCAO model (28). Pax6 expression increased in hypoxic brain neuronal cells in previous studies (29,30). In the BCCAO model, Pax6 was used as an early neurogenic marker, whose increased expression implies improved neurogenesis (31).…”

Section: Discussionsupporting

confidence: 91%

Differential Expression of Pax6 Following Bilateral Common Carotid Artery Occlusion

Kim

Lee

Cho

et al. 2023

In Vivo

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Background/Aim: Chronic cerebral hypoperfusion causes neuronal damage involving cognitive impairment and development of dementia. Permanent bilateral common carotid artery occlusion (BCCAO) in rat models is used to study chronic cerebral hypoperfusion. Pax6 is used as an early neurogenesis marker which affects the maturation of neuronal cells. However, the expression of PAX 6 after BCCAO is not well understood. In this study, we investigated the expression of PAX6 in the neurogenic zones after BCCAO to evaluate the effects of Pax6 on chronic hypoperfusion. Materials and Methods: Chronic hypoperfusion was induced by BCCAO. Common carotid artery was laid parallel to the vagus nerve and separated from it. Both arteries were occluded using 4-0 silk sutures. Rats who underwent bicommon carotid artery occlusion formed in the BCCAO group, while unoperated rats served as the control group. Brain samples were obtained on days 3 and 14 after BCCAO and subjected to immunohisto-chemistry with NeuN and western blotting for Pax6 and HIF1α. Results: Compared to the control, the expression of Pax6 increased three days after surgery but did not differ on day 14, while that of NeuN showed the opposite trend. The expression of HIF1α increased three days after surgery. Conclusion: Bilateral common carotid artery occlusion induced early neurogenesis at three days after BCCAO but this result was not maintained at fourteen days after BCCAO.

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Section: Discussionsupporting

confidence: 91%

Differential Expression of Pax6 Following Bilateral Common Carotid Artery Occlusion

Kim

Lee

Cho

et al. 2023

In Vivo

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“…According to several studies, ischemia stimulates neurogenesis in both rodents [ 253 ] and primates [ 254 ]. In the ipsilateral SVZ, activated microglia with cellular processes facilitate the migration of neuronal precursor cells, while amoeboid microglia in the peri-infarct zone may have an adverse effect on neurogenesis [ 255 ].…”

Section: Ischemic Brain Injurymentioning

confidence: 99%

Glial Populations in the Human Brain Following Ischemic Injury

Mihailova,

Stoyanova,

Tonchev

2023

Biomedicines

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There is a growing interest in glial cells in the central nervous system due to their important role in maintaining brain homeostasis under physiological conditions and after injury. A significant amount of evidence has been accumulated regarding their capacity to exert either pro-inflammatory or anti-inflammatory effects under different pathological conditions. In combination with their proliferative potential, they contribute not only to the limitation of brain damage and tissue remodeling but also to neuronal repair and synaptic recovery. Moreover, reactive glial cells can modulate the processes of neurogenesis, neuronal differentiation, and migration of neurons in the existing neural circuits in the adult brain. By discovering precise signals within specific niches, the regulation of sequential processes in adult neurogenesis holds the potential to unlock strategies that can stimulate the generation of functional neurons, whether in response to injury or as a means of addressing degenerative neurological conditions. Cerebral ischemic stroke, a condition falling within the realm of acute vascular disorders affecting the circulation in the brain, stands as a prominent global cause of disability and mortality. Extensive investigations into glial plasticity and their intricate interactions with other cells in the central nervous system have predominantly relied on studies conducted on experimental animals, including rodents and primates. However, valuable insights have also been gleaned from in vivo studies involving poststroke patients, utilizing highly specialized imaging techniques. Following the attempts to map brain cells, the role of various transcription factors in modulating gene expression in response to cerebral ischemia is gaining increasing popularity. Although the results obtained thus far remain incomplete and occasionally ambiguous, they serve as a solid foundation for the development of strategies aimed at influencing the recovery process after ischemic brain injury.

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“…According to several studies, ischemia stimulates neurogenesis in both rodents [253] and primates [254]. In the ipsilateral SVZ, activated microglia with cellular processes facilitate the migration of neuronal precursor cells, while amoeboid microglia in the periinfarct zone may have an adverse effect on neurogenesis [255].…”

Section: Role Of Oligodendrocytes In Ischemic Brain Injurymentioning

confidence: 99%

Glial Populations in the Human Brain Following Ischemic Injury

Mihailova¹,

Stoyanova²,

Tonchev³

2023

Preprint

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There is a growing interest in glial cells in the central nervous system due to their important role in maintaining brain homeostasis both under physiological conditions and after injury. A significant amount of evidence has been accumulated regarding their capacity to exert either pro-inflammatory or anti-inflammatory effects under different pathological conditions. In combination with their known proliferative potential, they contribute not only to the limitation of brain damage and tissue remodeling but also to neuronal repair and synaptic recovery. Moreover, reactive glial cells can modulate the processes of neurogenesis, proliferation, and migration of neurons in the existing neural circuits in the adult brain. By discovering precise signals within specific niches, the regulation of sequential processes in adult neurogenesis holds the potential to unlock strategies that can stimulate the generation of functional neurons, whether in response to injury or as a means of addressing degenerative neurological conditions. Cerebral ischemic stroke, a condition falling within the realm of acute vascular disorders affecting the circulation of the brain, stands as a prominent global cause of disability and mortality. Extensive investigations into glial plasticity and their intricate interactions with other cells in the central nervous system have predominantly relied on studies conducted on experimental animals, including rodents and primates. However, valuable insights have also been gleaned from in vivo studies involving post-stroke patients, utilizing highly specialized imaging techniques. Following the attempts to map brain cells, the role of various transcription factors in modulating gene expression in response to cerebral ischemia is gaining increasing popularity. Although the results obtained thus far remain incomplete and occasionally ambiguous, they serve as a solid foundation for the development of strategies aimed at influencing the recovery process after ischemic brain injury.

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Ghrelin Regulates Expression of the Transcription Factor Pax6 in Hypoxic Brain Progenitor Cells and Neurons

Cited by 5 publications

References 105 publications

Differential Expression of Pax6 Following Bilateral Common Carotid Artery Occlusion

Differential Expression of Pax6 Following Bilateral Common Carotid Artery Occlusion

Glial Populations in the Human Brain Following Ischemic Injury

Glial Populations in the Human Brain Following Ischemic Injury

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