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Functions of Reactive Astrocytes in Ischemic Brain Injury

Yıl 2023, Cilt: 49 Sayı: 1, 133 - 143, 09.06.2023
https://doi.org/10.32708/uutfd.1261257

Öz

Stroke is the second leading cause of death worldwide. It is important to investigate the pathophysiology of astrocytes, which constitute the most common glial cell group in the mammalian central nervous system (CNS), in the acute and chronic stages of stroke. In pathological conditions following disease and brain damage, astrocytes transform into reactive form. It has been proven by studies that they alleviate oxidative stress damage by releasing GSH (Glutathione) after ischemic injury, contribute to neuron development and survival by secreting neurotrophic factors, have a role in the regulation of cerebral edema, and contribute to angiogenesis by secreting erythropoietin and inhibit neuronal apaptosis. However, besides all these, it has been shown that it causes neuronal death and increases the permeability of the BBB by inducing excitotoxicity after ischemia and causing excessive release of inflammatory factors. There are studies showing that the glial scar formed after ischemic injury provides homeostasis in healthy tissue by preventing the spread of tissue damage in the acute period, but prevents axon growth in the chronic period. Therefore, the functions of reactive astrocytes are controversial. It has been found that genetically reactive astrocytes can undergo transformation into two polarization states, neurotoxic (A1) and neuroprotective (A2). Different types of astrocytes will help discover effective treatment approaches for neurological diseases. In this review; the functions of reactive astrocytes in stroke caused by ischemic brain injury the physiological and histomorphological changes of astrocytes in this process are included.

Kaynakça

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İskemik Beyin Hasarında Reaktif Astrositlerin Fonksiyonları

Yıl 2023, Cilt: 49 Sayı: 1, 133 - 143, 09.06.2023
https://doi.org/10.32708/uutfd.1261257

Öz

İnme, dünya çapında ikinci önde gelen ölüm nedenidir. Memeli merkezi sinir sistemindeki (MSS) en yaygın glial hücre grubunu oluşturan astrositlerin inmenin akut ve kronik evresindeki patofizyolojilerinin araştırılması önemlidir. Hastalık ve beyin hasarlarını takiben görülen patolojik durumlarda astrositler reaktif forma dönüşürler. İskemik hasar sonrası Glutatyon (GSH) salgılayarak oksidatif stres hasarını hafiflettikleri, nörotrofik faktörler salgılayarak nöron gelişimi ve sağ kalımına katkıda bulundukları, serebral ödemin düzenlenmesinde rolleri olduğu ve eritropoietin salgılayarak anjiyogeneze katkı sağladığı ve nöronal apoptozu inhibe ettiği yapılan çalışmalarla kanıtlanmıştır. Ancak tüm bunların yanı sıra, iskemi sonrası eksitotoksisiteyi indükleyerek ve inflamatuar faktörlerin aşırı salınımına yol açarak nöronal ölüme yol açtığı ve kan-beyin bariyeri (KBB)’nin geçirgenliğini attırdığı gösterilmiştir. İskemik hasar sonrası oluşan glial skarın akut dönemde doku hasarının yayılmasını önleyerek sağlıklı dokudaki homeostazı sağladığı ancak kronik dönemde akson büyümesine engel olduğunu gösteren çalışmalar mevcuttur. Bu yüzden reaktif astrositlerin işlevleri tartışmalıdır. Genetik olarak reaktif astrositlerin nörotoksik (A1) ve nöroprotektif (A2) iki polarizasyon durumuna dönüşüm geçirebileceği bulunmuştur. Farklı astrosit tipleri nörolojik hastalıklar için etkili tedavi yaklaşımlarının keşfedilmesine yardımcı olacaktır. Bu derlemede; iskemik beyin hasarına bağlı olarak oluşan inmede reaktif astrositlerin fonksiyonlarına ve bu süreçte astrositlerin fizyolojik ve histomorfolojik değişimlerine yer verilmiştir.

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  • 131. Xiao W, Wang W, Chen W, et al. GDNF is involved in thebarrier-inducing effect of enteric glial cells on intestinal epithelial cells under acute ischemia reperfusion stimulation. Mol Neurobiol 2014;50:274-89.
  • 132. Al-Ahmady Z S. Selective drug delivery approaches to lesioned brain through blood brain barrier disruption. Expert Opin. Drug Deliv. 2018;15:335-49.
  • 133. Cohen E, Dillin A. The insulin paradox: aging, proteotoxicity and neurodegeneration. Nat Rev Neurosci 2008;9:759-67.
  • 134. Song Y, Pimentel C, Walters K, et al. Neuroprotective levels ofIGF-1 exacerbate epileptogenesis after brain injury. Sci Rep2016;6:32095.
  • 135. Iliff JJ, Wang M, Liao Y, et al. A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid β. Sci. Transl Med 2012; 4:147ra111.
  • 136. Nedergaard M. Neuroscience. garbage truck of the brain. Science 2013; 340:1529-30.
  • 137. Levison SW, Jiang FJ, Stoltzfus OK, Ducceschi MH. IL-6-type cytokines enhance epidermal growth factor-stimulated astrocyte proliferation. Glia 2000;32:328-37
  • 138. Gadea A, Schinelli S, Gallo V. Endothelin-1 regulates astrocyte proliferation and reactive gliosis via a JNK/c-Jun signaling pathway. J Neurosci 2008; 28:2394-2408.
  • 139. Neary JT, Zimmermann H. Trophic functions of nucleotides in the central nervous system. Trends Neurosci 2009;32:189-98.
  • 140. Faulkner JR, Herrmann JE, Woo M J, Tansey KE, Doan NB,Sofroniew MV. Reactive astrocytes protect tissue and preserve function after spinal cord injury. J Neurosci 2004;24:2143-55.
  • 141. Rolls A, Shechter R, Schwartz M. The bright side of the glial scar in CNS repair. Nat Rev Neurosci 2009;10:235-41.
  • 142. Bush TG, Puvanachandra N. Horner CH. et al. Leukocyteinfiltration, neuronal degeneration, and neurite outgrowth afterablation of scar-forming, reactive astrocytes in adult transgenic mice. Neuron 2014;23:297-308.
  • 143. Burda JE. Sofroniew MV. Reactive gliosis and the multicellularresponse to CNS damage and disease. Neuron 2014;81:229-48.
  • 144. Sofroniew MV. Multiple roles for astrocytes as effectors ofcytokines and inflammatory mediators. Neuroscientist 2014;20:160-72.
  • 145. Myer DJ, Gurkoff GG, Lee SM, Hovda D A, Sofroniew MV.Essential protective roles of reactive astrocytes in traumatic brain injury. Brain 2006;129:2761-72.
  • 146. Chung IY, Benveniste EN. Tumor necrosis factor-alpha production by astrocytes. induction by lipopolysaccharide, IFN-gamma, and IL-1 beta. J Immunol 1990;144:2999-3007.
  • 147. Yiu G, He, Z. Glial inhibition of CNS axon regeneration. Nat Rev Neurosci. 2006;7:617-27.
  • 148. Silver J, Schwab ME, Popovich PG. Central nervous systemregenerative failure: role of oligodendrocytes, astrocytes, and microglia. Cold Spring Harb. Perspect. Biol 2014;7:a020602
  • 149. Asher RA, Morgenstern RA, Moon LD. Fawcett JW.Chondroitin sulphate proteoglycans: inhibitory components of the glial scar Prog. Brain Res.2001;132:611-19.
  • 150. Liddelow S, Barres B. Reactive astrocytes: production, function, and therapeutic potential. Immunity 2017;46:957-67.
  • 151. King A, Szekely B, Calapkulu E, et al. The increased densities, but different distributions, of both C3 and S100A10immunopositive astrocyte-like cells in alzheimer’s disease brains suggest possible roles for both A1 and A2 astrocytes inthe disease pathogenesis. Brain Sci 2020;10:503.
  • 152. Zou LH, Shi YJ, He H, et al. Effects of FGF2/FGFR1 pathwayon expression of A1 astrocytes after infrasound exposure. Front Neurosci 2019;13:429.
Toplam 152 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Konular Sağlık Kurumları Yönetimi
Bölüm Derleme Makaleler
Yazarlar

Nursel Hasanoğlu Akbulut 0000-0001-5704-5793

Gonca Topal 0000-0003-0426-2684

Özhan Eyigör 0000-0003-3463-7483

Yayımlanma Tarihi 9 Haziran 2023
Kabul Tarihi 25 Mayıs 2023
Yayımlandığı Sayı Yıl 2023 Cilt: 49 Sayı: 1

Kaynak Göster

APA Hasanoğlu Akbulut, N., Topal, G., & Eyigör, Ö. (2023). İskemik Beyin Hasarında Reaktif Astrositlerin Fonksiyonları. Uludağ Üniversitesi Tıp Fakültesi Dergisi, 49(1), 133-143. https://doi.org/10.32708/uutfd.1261257
AMA Hasanoğlu Akbulut N, Topal G, Eyigör Ö. İskemik Beyin Hasarında Reaktif Astrositlerin Fonksiyonları. Uludağ Tıp Derg. Haziran 2023;49(1):133-143. doi:10.32708/uutfd.1261257
Chicago Hasanoğlu Akbulut, Nursel, Gonca Topal, ve Özhan Eyigör. “İskemik Beyin Hasarında Reaktif Astrositlerin Fonksiyonları”. Uludağ Üniversitesi Tıp Fakültesi Dergisi 49, sy. 1 (Haziran 2023): 133-43. https://doi.org/10.32708/uutfd.1261257.
EndNote Hasanoğlu Akbulut N, Topal G, Eyigör Ö (01 Haziran 2023) İskemik Beyin Hasarında Reaktif Astrositlerin Fonksiyonları. Uludağ Üniversitesi Tıp Fakültesi Dergisi 49 1 133–143.
IEEE N. Hasanoğlu Akbulut, G. Topal, ve Ö. Eyigör, “İskemik Beyin Hasarında Reaktif Astrositlerin Fonksiyonları”, Uludağ Tıp Derg, c. 49, sy. 1, ss. 133–143, 2023, doi: 10.32708/uutfd.1261257.
ISNAD Hasanoğlu Akbulut, Nursel vd. “İskemik Beyin Hasarında Reaktif Astrositlerin Fonksiyonları”. Uludağ Üniversitesi Tıp Fakültesi Dergisi 49/1 (Haziran 2023), 133-143. https://doi.org/10.32708/uutfd.1261257.
JAMA Hasanoğlu Akbulut N, Topal G, Eyigör Ö. İskemik Beyin Hasarında Reaktif Astrositlerin Fonksiyonları. Uludağ Tıp Derg. 2023;49:133–143.
MLA Hasanoğlu Akbulut, Nursel vd. “İskemik Beyin Hasarında Reaktif Astrositlerin Fonksiyonları”. Uludağ Üniversitesi Tıp Fakültesi Dergisi, c. 49, sy. 1, 2023, ss. 133-4, doi:10.32708/uutfd.1261257.
Vancouver Hasanoğlu Akbulut N, Topal G, Eyigör Ö. İskemik Beyin Hasarında Reaktif Astrositlerin Fonksiyonları. Uludağ Tıp Derg. 2023;49(1):133-4.

ISSN: 1300-414X, e-ISSN: 2645-9027

Uludağ Üniversitesi Tıp Fakültesi Dergisi "Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License" ile lisanslanmaktadır.


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Journal of Uludag University Medical Faculty is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

2023