Cystatin C and apolipoprotein E immunoreactivities in CA1 neurons in ischemic gerbil hippocampus

Ishimaru, Hirohisa; Ishikawa, Koichi; Ohe, Yoshihide; Takahashi, Akira; Maruyama, Yūji

doi:10.1016/0006-8993(95)01232-x

Cited by 51 publications

(34 citation statements)

References 39 publications

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“…Enhanced CysC expression is also shown in a 6-hydroxydopamine-induced Parkinson's disease model, while CysC rescued nigral dopaminergic neurons (Xu et al 2005). Recent studies also show the association of CysC with stroke (Palm et al 1995;Ishimaru et al 1996;Pirttila and Pitkanen 2006;Ni et al 2007;Xiao et al 2012). The CysC level in hippocampus increases after ischemic injury in different animal models (Palm et al 1995;Ishimaru et al 1996;Pirttila and Pitkanen 2006).…”

Section: Introductionmentioning

confidence: 91%

“…Recent studies also show the association of CysC with stroke (Palm et al 1995;Ishimaru et al 1996;Pirttila and Pitkanen 2006;Ni et al 2007;Xiao et al 2012). The CysC level in hippocampus increases after ischemic injury in different animal models (Palm et al 1995;Ishimaru et al 1996;Pirttila and Pitkanen 2006). High serum CysC is found in stroke patients and is associated with larger infarct size and hemorrhage volume (Ni et al 2007;Xiao et al 2012).…”

Section: Introductionmentioning

confidence: 94%

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Cystatin C is an Independent Risk Factor and Therapeutic Target for Acute Ischemic Stroke

et al. 2015

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Cystatin C (CysC) has been used as a renal function indicator and a strong predictor of cardiovascular events. In this study, we determined the prognostic value of serum CysC in patients with acute ischemic stroke (AIS) and examined its protective role on ischemic brain injury. First-ever stroke patients (601 cases) and control subjects (325 cases) were recruited. Serum CysC level in patients with AIS were significantly higher than that in controls. Multivariate logistic regression analyses showed that elevated CysC is an independent risk factor of AIS; the odds ratio (95 % confidence interval) was 9.80 (3.12-30.83). The integrated population was divided into quintiles according to serum CysC. Compared with the first quintile, the odds ratios of risk for AIS in fourth quintile and fifth quintile were 1.92 (1.08-3.40) and 2.88 (1.49-5.54), respectively. Serum CysC was not associated with neurological deficits and the location of ischemic area; however, serum CysC in patients decreased after one-week therapy. This was consistent with CysC expression after ischemia/reperfusion injury in a mouse focal ischemia/reperfusion injury model. Exogenous CysC exerted neuroprotective effects by reducing infarct volume in this animal stroke model. Therefore, serum CysC is highly associated with AIS and is an independent prediction marker for AIS. Since our findings demonstrated the protection of exogenous CysC on ischemic brain injury, CysC is a novel and promising therapeutic target for AIS.

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Section: Introductionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 94%

Cystatin C is an Independent Risk Factor and Therapeutic Target for Acute Ischemic Stroke

et al. 2015

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“…Cystatin C is expressed in degenerating hippocampal neurons following transient forebrain ischemia (Palm et al, 1995;Ishimaru et al, 1996), and has been reported to stimulate self-renewing, multipotent NSCs in vitro and neurogenesis in vivo (Taupin et al, 2000). Cystatin C is a strong endogenous inhibitor of lysosomal cysteine proteases, such as cathepsin B, L, H, and S (Taugner et al, 1985;Marks et al, 1986).…”

Section: Referencesmentioning

confidence: 99%

Stroke-Induced Neurogenesis: Physiopathology and Mechanisms

Taupin

2006

CNR

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Long-term disabilities are the main outcome of cerebral strokes, though some of the deficits show receding signs in the weeks and months following the "brain attack". Studies show that neurogenesis is induced in the hippocampus and subventricular zone (SVZ) in animal models of ischemia, and that new neurons are generated at the sites of degeneration, where they replace some of the lost nerve cells. The enhanced neurogenesis suggests the involvement of the hippocampus and SVZ in the physiopathology of cerebral strokes, and the generation of new neuronal cells at the sites of degeneration suggests that the central nervous system (CNS) may attempt to repair itself. In this manuscript, we will review the studies on adult neurogenesis in cerebral strokes, discuss the contribution of adult neurogenesis to the physiopathology of strokes, and its underlying mechanisms.

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“…Moreover, pathological overexpression of clusterin suggests that the synthesis of this protein was a result of selective delayed neuronal death rather than involvement in the pathological cascade of events that cause it (Walton et al, 1996). The pathological immunostaining for apolipoproteins A1, E, and J was shown extracellularly and intracellularly (Hall et al, 1995;Kida et al, 1995;Pluta et al, 1995a;Horsburgh, Nicoll 1996a, Horsburgh, Nicoll 1996bIshimaru et al, 1996b;Pluta 2000;Kamada et al, 2003). Intracellular staining was noted in damaged neurons exhibiting features of ischemic injury (Pluta 2000).…”

Section: Apolipoproteins After Ischemiamentioning

confidence: 99%