Potential Therapeutic Features of Human Amniotic Mesenchymal Stem Cells in Multiple Sclerosis: Immunomodulation, Inflammation Suppression, Angiogenesis Promotion, Oxidative Stress Inhibition, Neurogenesis Induction, MMPs Regulation, and Remyelination Stimulation

Abstract

Multiple sclerosis (MS) is an inflammatory and degenerative disorder of the central nervous system with unknown etiology. It is accompanied by demyelination of the nerves during immunological processes in the presence of oxidative stress, hypoxia, cerebral hypo-perfusion, and dysregulation in matrix metalloproteinases (MMPs). Human amniotic mesenchymal stem cells (hAMSCs) as pluripotent stem cells possess some conspicuous features which could be of therapeutic value in MS therapy. hAMSCs could mimic the cascade of signals and secrete factors needed for promoting formation of stable neovasculature and angiogenesis. hAMSCs also have immunomodulatory and immunosuppressive effects on inflammatory processes and reduce the activity of inflammatory cells, migration of microglia and inhibit recruitment of certain immune cells to injury sites. hAMSCs attenuate the oxidative stress supported by the increased level of antioxidant enzymes and the decreased level of lipid peroxidation products. Furthermore, hAMSCs enhance neuroprotection and neurogenesis in brain injuries by inhibition of inflammation and promotion of neurogenesis. hAMSCs could significantly increase the expression of neurotrophic factors, which prevents neurons from initiating programmed cell death and improves survival, development, and function of neurons. In addition, they induce differentiation of neural progenitor cells to neurons. hAMSCs could also inhibit MMPs dysregulation and consequently promote the survival of endothelial cells, angiogenesis and the stabilization of vascular networks. Considering the mentioned evidences, we hypothesized here that hAMSCs and their conditioned medium could be of therapeutic value in MS therapy due to their unique properties, including immunomodulation and inflammation suppression; angiogenesis promotion; oxidative stress inhibition; neurogenesis induction and neuroprotection; matrix metalloproteinases regulation; and remyelination stimulation.

A New Anabolic compound, LLP2A-Ale, Reserves Periodontal Bone Loss in Mice Through Augmentation of Bone Formation

“…Several studies have been conducted to test this approach in animal models of primary osteoporosis, aging, glucocorticoid-induced bone fragility, and fracture healing [8,10,11]. Our data, as well as those from others, have con rmed that MSCs have paracrine effects that reduce in ammation and restore angiogenesis and osteogenesis when they are localized within the bone microenvironment [11][12][13][14][15]. The current study aimed to for the study is to address the unmet medical needs for non-surgical therapy to reverse periodontal disease (PD)-induced bone loss, and test a new anabolic compound, LLP2A-Ale, in the treatment of PD-induced bone loss in a mouse model of PD.…”

TIPE2 Improves the immune tolerance of human amniotic mesenchymal stem cells

“…oxidative stress inhibition (Abbasi-Kangevari et al 2019). Tsuji et al (2010) found that the hAD-MSCs xenografted to cure myocardial ischemia-reperfusion injury will differentiate into myocardial cells and restore partial myocardial function without rejection (Tsuji et al 2010).…”

Modern Concepts in Regenerative Therapy for Ischemic Stroke: From Stem Cells for Promoting Angiogenesis to 3D-Bioprinted Scaffolds Customized via Carotid Shear Stress Analysis

“…Stem cells (SCs) are self-renewing and undifferentiated cells capable of differentiating into more than 200 types of cells. The potential therapeutic effect of SCs is related to their role in cell differentiation, inflammation, immunomodulation and the stimulation of endogenous repair processes, such as angiogenesis and neurogenesis [7,8,9]. SC therapy has emerged as an encouraging regenerative tool in modern medicine, with potential applications in ischemic stroke as well as in other neurodegenerative disorders [10,11].…”