Neuroprotection by urokinase plasminogen activator in the hippocampus

Cho, Eunsil; Lee, Kyung Jin; Seo, Jae Sung; Byun, Catherine Jeonghae; Chung, Sun-Ju; Suh, Dae Chul; Carmeliet, Peter; Koh, Jae‐Young; Kim, Jong Seung; Lee, Joo‐Yong

doi:10.1016/j.nbd.2012.01.010

Cited by 31 publications

(20 citation statements)

References 47 publications

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“…Previous studies using Plau-deficient mice or the uPA inhibitor UK122 suggested that uPA is neuroprotective [42,43]. In the present study, however, the lesion volume, ratio of ipsilateral to contralateral cortical volumes, and the rostrocaudal extent of the cortical lesion at 6 or 8 months post-CCI were similar between genotypes.…”

Section: Upa Deficiency Did Not Affect the Severity Of Post-cci Corticontrasting

confidence: 69%

Epileptogenesis after traumatic brain injury in Plau-deficient mice

Bolkvadze

Rantala

Puhakka

et al. 2015

Epilepsy & Behavior

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Section: Upa Deficiency Did Not Affect the Severity Of Post-cci Corticontrasting

confidence: 69%

Epileptogenesis after traumatic brain injury in Plau-deficient mice

Bolkvadze

Rantala

Puhakka

et al. 2015

Epilepsy & Behavior

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“…The results also suggest that aMUPA mice are protected against leptin resistance, a state that appears under chronic increase in leptin (Halaas et al 1997), such as during obesity (Montague et al 1997). Interestingly, FVB/N mice, which have been used as a diet-induced obesityresistant model (Kim et al 2012), also became obese, suggesting that these mice are not resistant to leptin antagonist-induced weight gain. Surprisingly, we found that the weight gain seen in all mice was associated with increased food intake only during the first week of PEG-SMLA injection, but decreased to levels only slightly higher than those consumed by saline-injected mice.…”

Section: Discussionmentioning

confidence: 74%

“…uPA is an extracellular serine protease that plays a role in fibrinolysis and tissue remodeling (Mondino & Blasi 2004) and has been implicated in brain development, synaptic plasticity, and neuroprotection (Del Bigio et al 1999, Cho et al 2012. aMUPA mice show transgenic expression in the ocular lens, as expected from the promoter specificity, however also ectopic expression specifically in the brain and developing teeth .…”

Section: Introductionmentioning

confidence: 99%

A superactive leptin antagonist alters metabolism and locomotion in high-leptin mice

Chapnik

Solomon

Genzer

et al. 2013

Journal of Endocrinology

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Transgenic alpha murine urokinase-type plasminogen activator (aMUPA) mice are resistant to obesity and their locomotor activity is altered. As these mice have high leptin levels, our objective was to test whether leptin is responsible for these characteristics. aMUPA, their genetic background control (FVB/N), and C57BL mice were injected s.c. every other day with 20 mg/kg pegylated superactive mouse leptin antagonist (PEG-SMLA) for 6 weeks. We tested the effect of PEG-SMLA on body weight, locomotion, and bone health. The antagonist led to a rapid increase in body weight and subsequent insulin resistance in all treated mice. Food intake of PEG-SMLA-injected animals increased during the initial period of the experiment but then declined to a similar level to that of the control animals. Interestingly, aMUPA mice were found to have reduced bone volume (BV) than FVB/N mice, although PEG-SMLA increased bone mass in both strains. In addition, PEG-SMLA led to disrupted locomotor activity and increased corticosterone levels in C57BL but decreased levels in aMUPA or FVB/N mice. These results suggest that leptin is responsible for the lean phenotype and reduced BV in aMUPA mice; leptin affects corticosterone levels in mice in a strain-specific manner; and leptin alters locomotor activity, a behavior determined by the central circadian clock.

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“…The expression of urokinase and BDNF in the area adjacent to the ischemic area of the nerve, provided with a trophic effect on the nerve fibers and facilitated more rapid recovery of their functions. In the literature there are data that urokinase and BDNF have a protective effect on brain neurons [19,20], but our findings allow us to extend the range of neuroprotective effect of these biologically active molecules on peripheral nerves.…”

Section: Pvax1-hbdnf and Pvax1-mupa Stimulate Nerve Recovery After Ismentioning

confidence: 78%