The Retina of Osteopontin deficient Mice in Aging

Ruzafa, Noelia; Pereiro, Xandra; Aspichueta, Patricia; Araiz, Javier; Vecino, Elena

doi:10.1007/s12035-017-0734-9

Cited by 19 publications

(22 citation statements)

References 64 publications

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“…Our results indicated that there was a correlation between αvβ3 and OPN, and a correlation between αvβ3 and SAβ-gal, and a correlation between OPN and SAβ-gal also presence. These were in line with the former studies [29][30][31].Due to the ligand-receptor relationship between OPN and αvβ3, we infer that elevated OPN through the αvβ3 integrin affect the SAβ-gal expression and in uence the cellular senescence.…”

Section: Discussionsupporting

confidence: 92%

The Expression of αvβ3 and Osteopontin in Articular Cartilage of Patients with Knee Osteoarthritis and Its Correlation with Disease Severity and Chondrosenescence

Cheng¹,

Tian²,

Gao³

et al. 2021

Preprint

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Background: Osteoarthritis(OA) is the most common joint pathological disease associated with aging,previous observations have revealed that both osteopontin (OPN) and αvβ3 integrin are expressed in chondrocytes and both could as the biomarker for the progression of knee OA .The research aimed to comprehend the expressions of OPN and αvβ3 integrin and the chondrocyte senescence levels in OA. Methods: 48 cartilage tissues from normal and knee OA patients were divided into four groups of normal,minor,moderate, severe lesions based on the Mankin score. Immunohistochemistry and western blot were used to determine the expresssions of αvβ3,OPN and SAβ-gal in articular cartilage,Then Spearman’s correlation was used to analyze the correlations between Mankin Scores and αvβ3, OPN and SAβ-gal. The pearson correlation analysis was used to analyze the correlation among the αvβ3, OPN and SAβ-gal. Results: The expression of OPN and αvβ3 and SAβ-gal in articular cartilage were explored. αvβ3, OPN and SAβ-gal proteins all elvated in OA cartilage, the correlation coefficient between the Mankin score and the average optical density value of αvβ3, OPN, SAβ-gal were r=0.60,r=0.75,r=0.87,respectively, all p＜0.001,the correlation between the average optical density value of αvβ3 and OPN was r=0.3191, p<0.05, the correlation between αvβ3 and SAβ-gal was r=0.4955, p<0.001 , the correlation between OPN and SAβ-gal was r=0.7821, p<0.001.Conclusion: the correlation between αvβ3 , OPN and SAβ-gal expression in articular cartilage might be important to the OA progression and pathogenesis. Nonetheless, more researches are needed to elucidate the exact contribution of αvβ3 , OPN and SAβ-gal in the degenerative process of OA.

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Section: Discussionsupporting

confidence: 92%

The Expression of αvβ3 and Osteopontin in Articular Cartilage of Patients with Knee Osteoarthritis and Its Correlation with Disease Severity and Chondrosenescence

Cheng¹,

Tian²,

Gao³

et al. 2021

Preprint

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“…Ascorbic acid-mediated increase in OPN in the cerebellum are linked with the positive effects of OPN in other studies which reported OPN-induced promotion of survival, proliferation, migration of neural stem cells and proliferation, and differentiation of glial cells into oligodendrocytes [15,39]. Additionally, OPN is required for normal retinal development, and OPN deficiency induces premature aging effects in the retina [40].…”

Section: Discussionmentioning

confidence: 99%

Effects of Ascorbic Acid on Osteopontin Expression and Axonal Myelination in the Developing Cerebellum of Lead-Exposed Rat Pups

Nam

Seo

Nahm

et al. 2019

IJERPH

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Osteopontin (OPN) is a multi-functional protein that binds to integrin and calcium-binding phosphoprotein. OPN is required for normal neuronal development and its axonal myelination. We studied the combined effect of lead (Pb) and ascorbic acid treatment on OPN expression in the developing cerebellum. We randomly divided pregnant female rats into three groups: control, Pb (lead acetate, 0.3%, drinking water), and Pb plus ascorbic acid (PA; ascorbic acid, 100 mg/kg, oral intubation) groups. The blood level of Pb was significantly increased, while ascorbic acid reduced Pb levels in the dams and pups. At postnatal day (PND) 21, results from Nissl staining and OPN immunohistochemistry demonstrated that OPN was detected in the Purkinje cell layer in the cerebellum. Ascorbic acid treatment mitigated Pb exposure-induced reduction in the number of intact Purkinje cells and OPN immunoreactive Purkinje cells in the cerebellum of pups. In addition, Pb-induced reduction in the number of oligodendrocytes and myelin-associated glycoprotein is associated with the malformation of the myelin sheath. Ascorbic acid provided protection from Pb-induced impairments. Pb-induced structural deficits in the cerebellum resulted in functional deterioration observed during locomotive tests (bar holding test and wire mesh ascending test), while ascorbic acid ameliorated these harmful effects. Present results suggest that the change of OPN is associated with myelination in the developing cerebellum. The results also demonstrated that exposure to Pb is harmful, while ascorbic acid treatment is beneficial.

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“…In addition to the role of OPN in cellular migration, recent studies have shown that astrocyte polarization is linked to the integrin subunit and that depletion of hematogenous OPN resulted in the defective polarization of reactive astrocytes in a photothrombic stroke model [14, 59]. Furthermore, OPN deficient mice exhibited attenuation of reactive astrogliosis after stab wound injury [27], while the absence of OPN in the retina displayed a deficit in astrocyte coverage and linear extension and process branching indicative of premature aging [28]. In this regard, OPN’s overlapping distribution and often direct contact with astrocytes at days 7–14 after the 3-NP injury indicate a probable direct interaction of OPN protein with scar-forming astroglia, possibly involving the modulation of process elongation and polarization.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, recent studies have shown that macrophage-secreted OPN induces the polarization of reactive astrocytes after stroke [14] and that OPN is essential for astrocyte activation in an injured mouse brain, as well as in the primary culture of astrocytes [27]. In addition, OPN is necessary for the cell adhesion, migration, and survival of retinal astrocytes [28] and regulates metabolic activity in cultured optic nerve head astrocytes [29]. Thus, OPN plays a functional role not only in microglia/macrophages, but also in the astroglial reaction elicited by CNS insults.…”

Section: Introductionmentioning

confidence: 99%

Osteopontin and its spatiotemporal relationship with glial cells in the striatum of rats treated with mitochondrial toxin 3-nitropropionic acid: possible involvement in phagocytosis

Riew

Kim

Jin

et al. 2019

J Neuroinflammation

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Background Osteopontin (OPN, SPP1) is upregulated in response to acute brain injury, and based on its immunoreactivity, two distinct forms have been identified: intracellular OPN within brain macrophages and small granular OPN, identified as OPN-coated degenerated neurites. This study investigates the spatiotemporal relationship between punctate OPN deposition and astroglial and microglial reactions elicited by 3-nitropropionic acid (3-NP). Methods Male Sprague-Dawley rats were intraperitoneally injected with mitochondrial toxin 3-NP and euthanized at 3, 7, 14, and 28 days. Quantitative and qualitative light and electron microscopic techniques were used to assess the relationship between OPN and glial cells. Statistical significance was determined by Student’s t test or a one-way analysis of variance followed by Tukey’s multiple comparisons test. Results Punctate OPN-immunoreactive profiles were synthesized and secreted by amoeboid-like brain macrophages in the lesion core, but not by reactive astrocytes and activated microglia with a stellate shape in the peri-lesional area. Punctate OPN accumulation was detected only in the lesion core away from reactive astrocytes in the peri-lesional area at day 3, but had direct contact with, and even overlapped with astroglial processes at day 7. The distance between the OPN-positive area and the astrocytic scar significantly decreased from days 3 to 7. By days 14 and 28 post-lesion, when the glial scar was fully formed, punctate OPN distribution mostly overlapped with the astrocytic scar. Three-dimensional reconstructions and quantitative image analysis revealed numerous granular OPN puncta inside the cytoplasm of reactive astrocytes and brain macrophages. Reactive astrocytes showed prominent expression of the lysosomal marker lysosomal-associated membrane protein 1, and ultrastructural analysis confirmed OPN-coated degenerating neurites inside astrocytes, suggesting the phagocytosis of OPN puncta by reactive astrocytes after injury. Conclusions Punctate OPN-immunoreactive profiles corresponded to OPN-coated degenerated neurites, which were closely associated with, or completely engulfed by, the reactive astrocytes forming the astroglial scar in 3-NP lesioned striatum, suggesting that OPN may cause astrocytes to migrate towards these degenerated neurites in the lesion core to establish physical contact with, and possibly, to phagocytose them. Our results provide novel insights essential to understanding the recovery and repair of the central nervous system tissue. Electronic supplementary material The online version of this article (10.1186/s12974-019-1489-1) contains supplementary material, which is available to authorized users.

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The Retina of Osteopontin deficient Mice in Aging

Cited by 19 publications

References 64 publications

The Expression of αvβ3 and Osteopontin in Articular Cartilage of Patients with Knee Osteoarthritis and Its Correlation with Disease Severity and Chondrosenescence

The Expression of αvβ3 and Osteopontin in Articular Cartilage of Patients with Knee Osteoarthritis and Its Correlation with Disease Severity and Chondrosenescence

Effects of Ascorbic Acid on Osteopontin Expression and Axonal Myelination in the Developing Cerebellum of Lead-Exposed Rat Pups

Osteopontin and its spatiotemporal relationship with glial cells in the striatum of rats treated with mitochondrial toxin 3-nitropropionic acid: possible involvement in phagocytosis

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