Antagonistic effects of ultra-low-molecular-weight heparin on Aβ25–35-induced apoptosis in cultured rat cortical neurons

Liu, Hao; Zhang, Qing-zhu; Yu, Tao; Cheng, Ye; Sheng-li, JI

doi:10.1016/j.brainres.2010.10.064

Cited by 28 publications

(12 citation statements)

References 43 publications

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“…showed that LMWH inhibits the TNF‐α‐induced apoptosis of decidual cells. Furthermore, other reports indicated that ultra‐LMWH increases cell viability and decreases the number of apoptotic cells as well as caspase‐3 activity . These observations were obtained in vitro after culturing either primary decidual cells or neurons .…”

Section: Discussionsupporting

confidence: 52%

Low Molecular Weight Heparin Modulates Maternal Immune Response in Pregnant Women and Mice with Thrombophilia

Luley

Schumacher

Mulla

et al. 2014

American J Rep Immunol

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Section: Discussionsupporting

confidence: 52%

Low Molecular Weight Heparin Modulates Maternal Immune Response in Pregnant Women and Mice with Thrombophilia

Luley

Schumacher

Mulla

et al. 2014

American J Rep Immunol

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“…Aβ25–35, which is a chemosynthesis product of toxic peptide fragment designed based on natural amyloid protein, was dissolved in deionized water and incubated with constant oscillation at 37 °C for 3 days to induce its aggregation [32]. After aggregation, the solution of Aβ25–35 was stored at −20 °C.…”

Section: Methodsmentioning

confidence: 99%

Protective Effects of Fucoidan on Aβ25–35 and d-Gal-Induced Neurotoxicity in PC12 Cells and d-Gal-Induced Cognitive Dysfunction in Mice

et al. 2017

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Alzheimer’s disease (AD) is a chronic neurodegenerative disease which contributes to memory loss and cognitive decline in the elderly. Fucoidan, extracted from brown algae, is a complex sulfated polysaccharide and potential bioactive compound. In this study, we investigated whether fucoidan protects PC12 cells from apoptosis induced by a combination of beta-amyloid 25–35 (Aβ25–35) and d-galactose (d-Gal), and improves learning and memory impairment in AD model mice. The results indicated that fucoidan could inhibit the release of cytochrome c from the mitochondria to cytosol and activation of caspases, and increase the expression of apoptosis inhibitor proteins (IAPs), including livin and X-linked IAP (XIAP) in PC12 cells damaged by Aβ25–35 and d-Gal-induction. Fucoidan reversed the decreased activity of acetylcholine (ACh) and choline acetyl transferase (ChAT), as well as the increased activity of acetylcholine esterase (AChE), in AD model mice induced by infusion of d-Gal. Furthermore, fucoidan improved antioxidant activity in vitro and in vivo by activation of superoxide dismutase (SOD) and glutathione (GSH). These results suggested that fucoidan could protect PC12 cells from apoptosis and ameliorate the learning and memory impairment in AD model mice, which appeared to be due to regulating the cholinergic system, reducing oxidative stress, and inhibiting the caspase-dependent apoptosis pathway.

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“…Previous studies reported the heparin‐dependent acceleration of fibrillation . Its protective effects against the depolymerization of preformed fibrils to produce cytotoxic oligomers have been demonstrated . In addition, the interaction between heparin molecules and amyloid fibrils have been also reported .…”

Section: Introductionmentioning

confidence: 90%

Heparin‐induced amyloid fibrillation of β₂‐microglobulin explained by solubility and a supersaturation‐dependent conformational phase diagram

Hata

Naiki

et al. 2017

Protein Science

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Amyloid fibrils are fibrillar deposits of denatured proteins associated with amyloidosis and are formed by a nucleation and growth mechanism. We revisited an alternative and classical view of amyloid fibrillation: amyloid fibrils are crystal-like precipitates of denatured proteins formed above solubility upon breaking supersaturation. Various additives accelerate and then inhibit amyloid fibrillation in a concentration-dependent manner, suggesting that the combined effects of stabilizing and destabilizing forces affect fibrillation. Heparin, a glycosaminoglycan and anticoagulant, is an accelerator of fibrillation for various amyloidogenic proteins. By using β -microglobulin, a protein responsible for dialysis-related amyloidosis, we herein examined the effects of various concentrations of heparin on fibrillation at pH 2. In contrast to previous studies that focused on accelerating effects, higher concentrations of heparin inhibited fibrillation, and this was accompanied by amorphous aggregation. The two-step effects of acceleration and inhibition were similar to those observed for various salts. The results indicate that the anion effects caused by sulfate groups are one of the dominant factors influencing heparin-dependent fibrillation, although the exact structures of fibrils and amorphous aggregates might differ between those formed by simple salts and matrix-forming heparin. We propose that a conformational phase diagram, accommodating crystal-like amyloid fibrils and glass-like amorphous aggregates, is important for understanding the effects of various additives.

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Antagonistic effects of ultra-low-molecular-weight heparin on Aβ25–35-induced apoptosis in cultured rat cortical neurons

Cited by 28 publications

References 43 publications

Low Molecular Weight Heparin Modulates Maternal Immune Response in Pregnant Women and Mice with Thrombophilia

Low Molecular Weight Heparin Modulates Maternal Immune Response in Pregnant Women and Mice with Thrombophilia

Protective Effects of Fucoidan on Aβ25–35 and d-Gal-Induced Neurotoxicity in PC12 Cells and d-Gal-Induced Cognitive Dysfunction in Mice

Heparin‐induced amyloid fibrillation of β₂‐microglobulin explained by solubility and a supersaturation‐dependent conformational phase diagram

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Antagonistic effects of ultra-low-molecular-weight heparin on Aβ25–35-induced apoptosis in cultured rat cortical neurons

Cited by 28 publications

References 43 publications

Low Molecular Weight Heparin Modulates Maternal Immune Response in Pregnant Women and Mice with Thrombophilia

Low Molecular Weight Heparin Modulates Maternal Immune Response in Pregnant Women and Mice with Thrombophilia

Protective Effects of Fucoidan on Aβ25–35 and d-Gal-Induced Neurotoxicity in PC12 Cells and d-Gal-Induced Cognitive Dysfunction in Mice

Heparin‐induced amyloid fibrillation of β2‐microglobulin explained by solubility and a supersaturation‐dependent conformational phase diagram

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Heparin‐induced amyloid fibrillation of β₂‐microglobulin explained by solubility and a supersaturation‐dependent conformational phase diagram