Gonadal steroids prevent cell damage and stimulate behavioral recovery after transient middle cerebral artery occlusion in male and female rats

Dang, Jon; Mitkari, Bhimashankar; Kipp, Markus; Beyer, Cordian

doi:10.1016/j.bbi.2011.01.013

Cited by 116 publications

(122 citation statements)

References 78 publications

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“…Due to their neuroprotective effects, the use of estrogens has been proposed for the treatment of different neuropathologies as Alzheimer's disease (Amtul et al 2010), Parkinson's disease (Baraka et al 2011), ischemic stroke (Dang et al 2011), schizophrenia (Kulkarni et al 2010), and Huntington's disease (Túnez et al 2006). However, some epidemiological studies show no benefits on cognitive performance after hormone therapy (Coker et al 2010;Mulnard et al 2000;Shumaker et al 2004), so the subject is very controversial.…”

Section: Introductionmentioning

confidence: 99%

Aging and substitutive hormonal therapy influence in regional and subcellular distribution of ERα in female rat brain

Navarro

Valle

Ordóñez³

et al. 2012

AGE

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Estrogens are not only critical for sexual differentiation it is well-known for the role of 17β-estradiol (E2) in the adult brain modulating memory, learning, mood and acts as a neuroprotector. E2 exerts its actions through two classical receptors: estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ). The distribution of both receptors changes from one brain area to another, E2 being able to modulate their expression. Among the classical features of aging in humans, we find cognitive impairment, dementia, memory loss, etc. As estrogen levels change with age, especially in females, it is important to know the effects of low E2 levels on ERα distribution; results from previous studies are controversial regarding this issue. In the present work, we have studied the effects of long-term E2 depletion as well as the ones of E2 treatment on ERα brain distribution of ovariectomized rats along aging in the diencephalon and in the telencephalon. We have found that ovariectomy causes downregulation and affects subcellular localization of ERα expression during aging, meanwhile prolonged estrogen treatment produces upregulation and overexpression of the receptor levels. Our results support the idea of the region-specific neuroprotection mechanisms mediated by estradiol.

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Section: Introductionmentioning

confidence: 99%

Aging and substitutive hormonal therapy influence in regional and subcellular distribution of ERα in female rat brain

Navarro

Valle

Ordóñez³

et al. 2012

AGE

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show abstract

“…As abovementioned, the earliest rodent studies on the effects of estrogens on ischemic stroke showed protective effects, and the vast majority of the later studies also corroborated this (e.g. [97][98][99] Several suggestions have been put forth as to why the results differ, in animals and humans alike. Perhaps the theory that has received the most attention is referred to as the "timing hypothesis" (or the window of opportunity hypothesis).…”

Section: Estrogens and Cerebral Ischemiamentioning

confidence: 70%

Challenges in experimental stroke research : The 17β-estradiol example

Ingberg¹

2016

Linköping University Medical Dissertations

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“…The procedure of tMCAO operation was performed as previously described (Dang et al 2011;Ulbrich et al 2012). Briefly, 12-week-old male Wistar rats (300-350 g) were anesthetized with 2% isoflurane (Abbott, Germany), and the regional cerebral blood flow (CBF) was measured on the ipsiand contralateral side during the whole procedure using Laser Doppler Flowmetry (Moor Instruments VMS-LDF2, UK).…”

Section: Methods Tmcaomentioning

confidence: 99%

“…RNA from the peri-infarct area and control tissue was isolated with the NucleoSpin® RNA/Protein Kit (Machery-Nagel, Germany) as described previously (Dang et al 2011). Purity of the RNA was controlled using 260:280 OD ratios (NanoDrop 1000, Peqlab, Germany).…”

Section: Rna Isolation and Cdna Synthesismentioning

confidence: 99%

Upregulation and phosphorylation of HspB1/Hsp25 and HspB5/αB-crystallin after transient middle cerebral artery occlusion in rats

Bartelt-Kirbach

Slowik

Beyer

et al. 2017

Cell Stress and Chaperones

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Ischemic stroke leads to cellular dysfunction, cell death, and devastating clinical outcomes. The cells of the brain react to such a cellular stress by a stress response with an upregulation of heat shock proteins resulting in activation of endogenous neuroprotective capacities. Several members of the family of small heat shock proteins (HspBs) have been shown to be neuroprotective. However, yet no systematic study examined all HspBs during cerebral ischemia. Here, we performed a comprehensive comparative study comprising all HspBs in an animal model of stroke, i.e., 1 h transient middle cerebral artery occlusion followed by 23 h of reperfusion. On the mRNA level out of the 11 HspBs investigated, HspB1/Hsp25, HspB3, HspB4/αA-crystallin, HspB5/αB-crystallin, HspB7/cvHsp, and HspB8/Hsp22 were significantly upregulated in the peri-infarct region of the cerebral cortex of infarcted hemispheres. HspB1 and HspB5 reached the highest mRNA levels and were also upregulated at the protein level, suggesting that these HspBs might be functionally most relevant. Interestingly, in the infarcted cortex, both HspB1 and HspB5 were mainly allocated to neurons and to a lesser extent to glial cells. Additionally, both proteins were found to be phosphorylated in response to ischemia. Our data suggest that among all HspBs, HspB1 and HspB5 might be most important in the neuronal stress response to ischemia/reperfusion injury in the brain and might be involved in neuroprotection.

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Gonadal steroids prevent cell damage and stimulate behavioral recovery after transient middle cerebral artery occlusion in male and female rats

Cited by 116 publications

References 78 publications

Aging and substitutive hormonal therapy influence in regional and subcellular distribution of ERα in female rat brain

Aging and substitutive hormonal therapy influence in regional and subcellular distribution of ERα in female rat brain

Challenges in experimental stroke research : The 17β-estradiol example

Upregulation and phosphorylation of HspB1/Hsp25 and HspB5/αB-crystallin after transient middle cerebral artery occlusion in rats

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