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000181679 041__ $$aEnglish
000181679 082__ $$a610
000181679 1001_ $$aPekna, Marcela$$b0
000181679 245__ $$aAstrocyte Responses to Complement Peptide C3a are Highly Context-Dependent.
000181679 260__ $$aDordrecht [u.a.]$$bSpringer Science + Business Media B.V$$c2023
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000181679 500__ $$a2023 Apr;48(4):1233-1241
000181679 520__ $$aAstrocytes perform a range of homeostatic and regulatory tasks that are critical for normal functioning of the central nervous system. In response to an injury or disease, astrocytes undergo a pronounced transformation into a reactive state that involves changes in the expression of many genes and dramatically changes astrocyte morphology and functions. This astrocyte reactivity is highly dependent on the initiating insult and pathological context. C3a is a peptide generated by the proteolytic cleavage of the third complement component. C3a has been shown to exert neuroprotective effects, stimulate neural plasticity and promote astrocyte survival but can also contribute to synapse loss, Alzheimer's disease type neurodegeneration and blood-brain barrier dysfunction. To test the hypothesis that C3a elicits differential effects on astrocytes depending on their reactivity state, we measured the expression of Gfap, Nes, C3ar1, C3, Ngf, Tnf and Il1b in primary mouse cortical astrocytes after chemical ischemia, after exposure to lipopolysaccharide (LPS) as well as in control naïve astrocytes. We found that C3a down-regulated the expression of Gfap, C3 and Nes in astrocytes after ischemia. Further, C3a increased the expression of Tnf and Il1b in naive astrocytes and the expression of Nes in astrocytes exposed to LPS but did not affect the expression of C3ar1 or Ngf. Jointly, these results provide the first evidence that the complement peptide C3a modulates the responses of astrocytes in a highly context-dependent manner.
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000181679 650_7 $$2Other$$aGene expression
000181679 650_7 $$2Other$$aGlia
000181679 650_7 $$2Other$$aIschemia
000181679 650_7 $$2Other$$aLipopolysaccharide
000181679 650_7 $$2Other$$aNeurodegeneration
000181679 7001_ $$0P:(DE-He78)a0206cc58a953ec87e0baa6eaaa9863c$$aSiqin, Sumen$$b1$$udkfz
000181679 7001_ $$ade Pablo, Yolanda$$b2
000181679 7001_ $$aStokowska, Anna$$b3
000181679 7001_ $$aTorinsson Naluai, Åsa$$b4
000181679 7001_ $$aPekny, Milos$$b5
000181679 773__ $$0PERI:(DE-600)2018503-0$$a10.1007/s11064-022-03743-5$$n4$$p1233-1241$$tNeurochemical research$$v48$$x0364-3190$$y2023
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