Osteopontin Expression during Early Cerebral Ischemia-Reperfusion in Rats: Enhanced Expression in the Right Cortex Is Suppressed by Acetaminophen

Baliga, Sunanda S.; Merrill, Gary F.; Shinohara, Mari L.; Denhardt, David T.

doi:10.1371/journal.pone.0014568

Cited by 15 publications

(8 citation statements)

References 46 publications

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“…Notably, Baliga et al . proposed that the intracellular form of OPN is increased in the cytoplasm of the cortex during early cerebral ischaemia-reperfusion, suggesting a role of OPN as a responder to stroke-induced cell damage83. Thus, we speculate that degenerating neurons could be the initial source of the OPN protein localised within dendritic mitochondria, but it remains to be established whether this indeed reflects the presence of intracellular OPN.…”

Section: Discussionmentioning

confidence: 75%

Spatiotemporal expression of osteopontin in the striatum of rats subjected to the mitochondrial toxin 3-nitropropionic acid correlates with microcalcification

Riew

Kim

Jin

et al. 2017

Sci Rep

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Our aim was to elucidate whether osteopontin (OPN) is involved in the onset of mineralisation and progression of extracellular calcification in striatal lesions due to mitochondrial toxin 3-nitropropionic acid exposure. OPN expression had two different patterns when observed using light microscopy. It was either localised to the Golgi complex in brain macrophages or had a small granular pattern scattered in the affected striatum. OPN labelling tended to increase in number and size over a 2-week period following the lesion. Ultrastructural investigations revealed that OPN is initially localised to degenerating mitochondria within distal dendrites, which were then progressively surrounded by profuse OPN on days 7–14. Electron probe microanalysis of OPN-positive and calcium-fixated neurites indicated that OPN accumulates selectively on the surfaces of degenerating calcifying dendrites, possibly via interactions between OPN and calcium. In addition, 3-dimensional reconstruction of OPN-positive neurites revealed that they are in direct contact with larger OPN-negative degenerating dendrites rather than with fragmented cell debris. Our overall results indicate that OPN expression is likely to correlate with the spatiotemporal progression of calcification in the affected striatum, and raise the possibility that OPN may play an important role in the initiation and progression of microcalcification in response to brain insults.

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Section: Discussionmentioning

confidence: 75%

Spatiotemporal expression of osteopontin in the striatum of rats subjected to the mitochondrial toxin 3-nitropropionic acid correlates with microcalcification

Riew

Kim

Jin

et al. 2017

Sci Rep

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“…[86][87][88] Previous studies have demonstrated that OPN is involved in iNOS pathway. 50,89,90 Induced OPN provides a dose-dependent pattern suppressing iNOS expression after acute brain injury 65,80 by increasing expression of integrin-β1 and then inhibiting the Janus kinase/signal transducers and activators of transcription…”

Section: Opn and Neuroinflammationmentioning

confidence: 99%

Osteopontin as a candidate of therapeutic application for the acute brain injury

Zhou

Yao

Sheng

et al. 2020

J Cellular Molecular Medi

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Acute brain injury is the leading cause of human death and disability worldwide, which includes intracerebral haemorrhage, subarachnoid haemorrhage, cerebral ischaemia, traumatic brain injury and hypoxia‐ischaemia brain injury. Currently, clinical treatments for neurological dysfunction of acute brain injury have not been satisfactory. Osteopontin (OPN) is a complex adhesion protein and cytokine that interacts with multiple receptors including integrins and CD44 variants, exhibiting mostly neuroprotective roles and showing therapeutic potential for acute brain injury. OPN‐induced tissue remodelling and functional repair mainly rely on its positive roles in the coordination of pro‐inflammatory and anti‐inflammatory responses, blood‐brain barrier maintenance and anti‐apoptotic actions, as well as other mechanisms such as affecting the chemotaxis and proliferation of nerve cells. The blood OPN strongly parallel with the OPN induced in the brain and can be used as a novel biomarker of the susceptibility, severity and outcome of acute brain injury. In the present review, we summarized the molecular signalling mechanisms of OPN as well as its overall role in different kinds of acute brain injury.

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“…The upregulation of OPN has been reported in rat retina that activated microglia on I–R, 11 in cardiomyocytes in an ex-vivo hemoperfused working porcine heart model, 12 in the brain during early cerebral I–R in rats 13 but also in cultured rat aortic vascular smooth muscle cells in response to hypoxia. 14 The role of OPN in I–R injury has largely been reported in the kidney and could have an unexpected protective and deleterious role.…”

mentioning

confidence: 92%

Osteopontin deficiency aggravates hepatic injury induced by ischemia–reperfusion in mice

et al. 2014

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Osteopontin (OPN) is a multifunctional protein involved in hepatic steatosis, inflammation, fibrosis and cancer progression. However, its role in hepatic injury induced by ischemia–reperfusion (I–R) has not yet been investigated. We show here that hepatic warm ischemia for 45 min followed by reperfusion for 4 h induced the upregulation of the hepatic and systemic level of OPN in mice. Plasma aspartate aminotransferase and alanine aminotransferase levels were strongly increased in Opn−/− mice compared with wild-type (Wt) mice after I–R, and histological analysis of the liver revealed a significantly higher incidence of necrosis of hepatocytes. In addition, the expression levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNFα), interleukin 6 (IL6) and interferon-γ were strongly upregulated in Opn−/− mice versus Wt mice after I–R. One explanation for these responses could be the vulnerability of the OPN-deficient hepatocyte. Indeed, the downregulation of OPN in primary and AML12 hepatocytes decreased cell viability in the basal state and sensitized AML12 hepatocytes to cell death induced by oxygen–glucose deprivation and TNFα. Further, the downregulation of OPN in AML12 hepatocytes caused a strong decrease in the expression of anti-apoptotic Bcl2 and in the ATP level. The hepatic expression of Bcl2 also decreased in Opn−/− mice versus Wt mice livers after I–R. Another explanation could be the regulation of the macrophage activity by OPN. In RAW macrophages, the downregulation of OPN enhanced iNOS expression in the basal state and sensitized macrophages to inflammatory signals, as evaluated by the upregulation of iNOS, TNFα and IL6 in response to lipopolysaccharide. In conclusion, OPN partially protects from hepatic injury and inflammation induced in this experimental model of liver I–R. This could be due to its ability to partially prevent death of hepatocytes and to limit the production of toxic iNOS-derived NO by macrophages.

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Osteopontin Expression during Early Cerebral Ischemia-Reperfusion in Rats: Enhanced Expression in the Right Cortex Is Suppressed by Acetaminophen

Cited by 15 publications

References 46 publications

Spatiotemporal expression of osteopontin in the striatum of rats subjected to the mitochondrial toxin 3-nitropropionic acid correlates with microcalcification

Spatiotemporal expression of osteopontin in the striatum of rats subjected to the mitochondrial toxin 3-nitropropionic acid correlates with microcalcification

Osteopontin as a candidate of therapeutic application for the acute brain injury

Osteopontin deficiency aggravates hepatic injury induced by ischemia–reperfusion in mice

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