Stanniocalcin 1 is important for poststroke functionality, but dispensable for ischemic tolerance

Tolvanen, A. Durukan; Westberg, Johan A.; Serlachius, Martina; Chang, Andy; Reddel, Roger R.; Andersson, Leif C.; Tatlısumak, Turgut

doi:10.1016/j.neuroscience.2012.10.062

Cited by 30 publications

(28 citation statements)

References 28 publications

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“…The biological function of STC-1 as a key regulator of neuronal calcium homeostasis 16 , the potential association of dysregulated calcium homeostasis with neurodegenerative diseases, 17,18 and the increased STC-1 expression in cerebrovascular disease 13,19 led us to hypothesize that the STC-1 concentration in CSF could be altered in AD and/or other neurodegenerative diseases. We found that: 1) STC-1 was readily measureable in CSF using a well established ELISA,…”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal Fluid Stanniocalcin-1 as a Biomarker for Alzheimer’s Disease and Other Neurodegenerative Disorders

et al. 2016

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Stanniocalcin-1 (STC-1) is a nerve cell-enriched protein involved in intracellular calcium homeostasis regulation. Changes in calcium regulation are hypothesized to play a role in the pathophysiology of Alzheimer's disease (AD). The expression of STC-1 increases in response to ischemic stroke, but whether it is altered in neurodegenerative disorder, particularly Alzheimer's disease (AD), has not been investigated before. We measured STC-1 in cerebrospinal fluid (CSF) samples from a total of 163 individuals including AD, prodromal AD (pAD), mixed AD, stable mild cognitive impairment (sMCI), and diagnoses of other dementia than AD, as well as cognitively normal controls (CNC) enrolled at academic centers in France and Sweden. STC-1 concentration was reliably measureable in all CSF samples and was significantly increased in the initial exploratory cohort of neurochemically enriched AD patients versus AD biomarker-negative controls. In the second cohort, STC-1 was increased in AD versus pAD, and other dementia disorders, but the difference was not statistically significant. In the third cohort, there was no significant difference in STC-1 concentration between AD and CNC; however, STC-1 concentration was significantly decreased in patients with other dementia disorders compared with AD and CNC. Taken together, CSF STC-1 showed an increasing trend in AD, but the findings were not consistent across the three study cohorts. In contrast, CSF STC-1 concentrations were reduced in patients with dementia diagnoses other than AD, as compared with both AD patients and CNC. The findings from these studies suggest CSF STC-1 as a potential biomarker in differential diagnosis of dementias.

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Section: Discussionmentioning

confidence: 99%

Cerebrospinal Fluid Stanniocalcin-1 as a Biomarker for Alzheimer’s Disease and Other Neurodegenerative Disorders

et al. 2016

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“…37 Functionally, STC-1 has been associated with calcium uptake, 38 hypoxic preconditioning, 39,40 and antioxidative stress properties through suppression of reactive oxygen species. 25,41–45 Additionally, STC-1 has also been shown to be neuroprotective for neurons, photoreceptors, and retinal ganglion cells, 26,46–48 and has been linked to anti-inflammatory effects by inhibiting macrophage chemotaxis, modulating transendothelial migration of leukocytes and reducing T cell infiltration. 23,45,49,50 …”

Section: Discussionmentioning

confidence: 99%

Stanniocalcin-1 Is an Ocular Hypotensive Agent and a Downstream Effector Molecule That Is Necessary for the Intraocular Pressure–Lowering Effects of Latanoprost

Roddy

Viker

Winkler

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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PurposeTo identify downstream signaling molecules through which intraocular pressure (IOP) is lowered following treatment with the prostaglandin analog latanoprost.MethodsTotal RNA and protein isolated from primary human Schlemm's canal cells (n = 3) treated with latanoprost (free acid; 100 nM) were processed for quantitative PCR and Western blot analysis. IOP was evaluated in stanniocalcin-1 (STC-1−/−) and wild-type mice following treatment with latanoprost or Rho kinase inhibitor Y27632. Human anterior segment pairs (n = 8) were treated with recombinant STC-1 (5, 50, or 500 ng/mL) and pressure was recorded using custom-designed software. The effect of recombinant STC-1 (0.5 mg/mL) on IOP was evaluated in wild-type mice. Tissue morphology was evaluated by light and transmission electron microscopy.ResultsIncreased STC-1 mRNA (4.0- to 25.2-fold) and protein expression (1.9- to 5.1-fold) was observed within 12 hours following latanoprost treatment. Latanoprost reduced IOP in wild-type mice (22.0% ± 1.9%), but had no effect on STC-1−/− mice (0.5% ± 0.7%). In contrast, Y27632 reduced IOP in both wild-type (12.5% ± 1.2%) and in STC-1−/− mice (13.1% ± 2.8%). Human anterior segments treated with STC-1 (500 ng/mL) showed an increase in outflow facility (0.15 ± 0.03 to 0.27 ± 0.09 μL/min/mm Hg) while no change was observed in paired vehicle-treated controls. Recombinant STC-1 reduced IOP in wild-type mice by 15.2% ± 3.0%. No observable morphologic changes were identified between treatment groups when evaluated by microscopy.ConclusionsLatanoprost-induced reduction of IOP is mediated through the downstream signaling molecule STC-1. When used by itself, STC-1 exhibits ocular hypotensive properties.

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“…To examine the effects of high altitude on the BBB, we evaluated permeability to EB 12. Six rats were anesthetized and then placed in a stereotactic apparatus; a 2% EB solution was injected slowly into the caudal vein.…”

Section: Methodsmentioning

confidence: 99%

Characteristics of a rat model of an open craniocerebral injury at simulated high altitude

Yu¹,

Xu²,

Hu³

et al. 2014

NeuroReport

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To establish a rat model of an open craniocerebral injury at simulated high altitude and to examine the characteristics of this model. Rats were divided randomly into a normobaric group and a high-altitude group and their corresponding control groups. A rat model of an open craniocerebral injury was established with a nail gun shot. Simulated high-altitude conditions were established with a hypobaric chamber at 0.6 ATA to mimic pressure at an altitude of 4000 m. Mortality, brain water content (BWC), Evans blue content, pathology, regional cerebral blood flow (rCBF), partial pressure of brain tissue oxygen (PbtO2), and brainstem auditory-evoked potential were observed after injury. The mortality of the high-altitude group was significantly greater than that of the normobaric group within 72 h after injury (P<0.05). BWC and Evans blue content increased by 48 h after injury (P<0.05); pathological changes in damaged brains were more serious. In contrast, rCBF and PbtO2 had decreased markedly by 72 h (P<0.01); brainstem auditory-evoked potential values were significantly prolonged (P<0.05). Moreover, an inverse correlation between rCBF and BWC and a positive correlation between rCBF and PbtO2 were found. The rat model of an open craniocerebral injury at simulated high altitude can be established successfully using a nail gun shot and a hypobaric chamber. The injury characteristics at high altitude were more serious, rapid, and prolonged than those in the normobaric group.

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Stanniocalcin 1 is important for poststroke functionality, but dispensable for ischemic tolerance

Cited by 30 publications

References 28 publications

Cerebrospinal Fluid Stanniocalcin-1 as a Biomarker for Alzheimer’s Disease and Other Neurodegenerative Disorders

Cerebrospinal Fluid Stanniocalcin-1 as a Biomarker for Alzheimer’s Disease and Other Neurodegenerative Disorders

Stanniocalcin-1 Is an Ocular Hypotensive Agent and a Downstream Effector Molecule That Is Necessary for the Intraocular Pressure–Lowering Effects of Latanoprost

Characteristics of a rat model of an open craniocerebral injury at simulated high altitude

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