Mini Review - Stem Cell Research and Regenerative Medicine (2023) Volume 6, Issue 3

Biological and Chromosomal Modifications of Advanced Multipotent Regenerative Cells

Lakshmi Shankar*

Department of Stem Cell and Research, Martinique

*Corresponding Author:
Lakshmi Shankar
Department of Stem Cell and Research, Martinique

Received: 01-June-2023, Manuscript No. srrm-23-102592; Editor assigned: 05-June-2023, Pre-QC No. srrm-23- 102592 (PQ); Reviewed: 19-June- 2023, QC No. srrm-23-102592; Revised: 24-June-2023, Manuscript No. srrm-23-102592 (R); Published: 30-June-2023, DOI: 10.37532/ srrm.2023.6(3).80-82



A person’s lifestyle has a significant impact on several significant epigenetic alterations that occur from the earliest stages of skeletal development throughout life as a result of ageing and disease. Epigenetics is the study of genetic changes in gene expression resulting from environmental changes without causing mutations in the underlying DNA sequences. Cellular epigenetic profiles are dynamic and mediated by a variety of mechanisms, including histone modifications, noncoding RNA-associated gene silencing, and DNA methylation. Considering the important role of dysfunctional mesenchymal tissue in common age-related skeletal diseases such as osteoporosis and osteoarthritis, skeletal stem cells or mesenchymal stem cells (MSCs) and their function during aging are, has been the subject of research into gene deregulation and how it mediates cellular senescence evolving epigenetic landscape. This review describes recent findings on epigenetic alterations in mesenchymal stem cells that influence growth and cell fate decisions associated with aging, nutrition, and exercise and bone disease.


Bone marrow stromal cells • Epigenetics • Osteogenic • Bone • Skeleton • Histone methylation


German pathologist Julius Kornheim first described the ability of rabbit and chicken bone marrow-derived fibroblast-like cells to form calcified ossicles when transplanted into muscle. . Nearly a century later, Friedenstein et al. reported the isolation and in vitro expansion of clonal adherent stromal progenitor cells from rodent bone marrow that could give rise to osteoblasts, adipocytes, and chondrocytes. bottom. . Colony-forming cells, so-called colony-forming unit fibroblasts (CFU-F), were later identified in human bone marrow aspirates [1]. Clonal analysis of ex vivo-expanded human CFU-F also revealed that it self-renews, supports the hematopoietic stem cell niche, promotes wound repair, and has immunomodulatory properties. These stromal progenitor cells were later called skeletal stem cells, mesenchymal stem/stromal cells (MSCs), stromal progenitor cells, and bone marrow-derived mesenchymal stromal cells (BMSCs) [2]. Although great progress has been made in identifying MSC-associated markers, no single cell surface marker could be identified as MSC-specific. STRO-1, CD44, CD49a, CD73, CD90, CD105, CD106, CD146, CD166, and CD271 are known to distinguish His-MSCs from many other cell types. Furthermore, the expression of these markers can be affected by culture conditions and passage number. Other selectable markers are leptin receptor+, PDGF receptor+, CXCL12+, α-smooth muscle actin+, Prx1+, nestin+, Mx1+, pluripotent cells with varying capacities to support hematopoiesis or take up reticulocyte pericyte. An alternative MSC isolation protocol is based on a negative selection approach to eliminate non- MSC accessory cells. CD200 and gremlin were recently shown to differentiate between osteoblastic and chondrocyte progenitor cell populations, but not between adipocytes [3]. Further studies have identified CFU-F or MSC-like populations found in other adult tissues such as adipose, dental pulp, gingiva and peripheral blood, which maintain tissue homeostasis and are important after injury, disease and aging acts as a reservoir of stem cells for repair. However, MSC-like populations derived from different tissues are known to exhibit different growth and developmental characteristics based on the epigenetic memory of each cell population, depending on the tissue of origin [4].

MSC’s biological changes

The skeleton is the major tissue that supports human structure and movement. It is also considered an endocrine organ responsible for maintaining calcium and glucose homeostasis [5]. Bone health is a major challenge in aging societies and common in developed countries where sedentary lifestyles are common. As a result, older people have lower bone density, increased rates of severe fractures and long-term severe disability, and mortality rates of 15-25%. Therefore, age has become a major risk factor for skeletal disease in developed countries. DNA damage, cellular stress responses, and both genomic and epigenomic alterations can lead to deterioration of homeostasis in healthy tissues, resulting in a variety of changes at both cellular and tissue levels [6]. The epigenetic context within stem cells is a dynamic process in which their ability to selfrenew and differentiate into functional organspecific cell types is progressively impaired with age. Consequently, the functional ability of mesenchymal stem cells to maintain tissue homeostasis is compromised by cellular senescence and senescence-associated phenotypic changes of mesenchymal stem cells, ultimately affecting their regenerative properties [7].

In postnatal organisms, BMSCs retain the ability to regenerate tissue after fractures, articular cartilage injuries, and other traumatic connective tissue injuries. Systemic inflammatory diseases such as osteoarthritis, osteoporosis and rheumatoid arthritis are among the most common and disabling degenerative musculoskeletal diseases and are often associated with aging. Other risk factors include obesity, alcohol consumption, smoking, a family history of femoral neck fractures, and joint trauma. Similar to other stem cell populations, there are multiple alterations in mesenchymal stem cell composition, function and structure due to intrinsic and extrinsic cellular senescence mechanisms [8]. Inherent aging mechanisms common to all cell types include impaired DNA repair, telomere shortening, altered gene expression, and epigenetic drift. With regard to the extrinsic mechanisms of cellular senescence, changes in tissue composition and microenvironment through hormone and growth factor signaling and increases in proinflammatory cytokines are thought to play important roles in mesenchymal stem cell senescence. . . Studies have shown that mesenchymal stem cells not only lose their osteogenic and chondrogenic differentiation potential with aging, but also undergo an adipogenic transition at the expense of osteogenic/chondrogenic differentiation gain. Thus, the transition to bone desorption impairs bone remodeling, increases cortical porosity, and thins trabeculae and cortex [9]. In addition, aged MSCs express less pro-inflammatory factors and exhibit reduced immunomodulatory capacity. This is associated with premature aging of MSCs. Endogenous signals cause “age-related mild inflammation known as ‘inflammation’” in the absence of noxious stimuli. Recent studies have shown that the number and function of mesenchymal stem cells influence bone healing. The role of inflammation in mitigating MSC aging, and in the development of therapeutics, hinges on understanding the molecular changes that cause MSC aging. One of the pillars of aging in all organisms is epigenetic drift, where changes in the epigenome lead to deregulation of cell proliferation and cell differentiation. Discovering key actors and their patterns of behavior is the focus of recent research [10].

Epigenetic regulation of MSC

Epigenetics are genetic alterations in gene expression that are not driven by DNA sequence changes and range from DNA methylation and histone modifications to noncoding RNA expression and changes in chromatin structure. These epigenetic alterations regulate gene expression by altering DNA accessibility to transcription factors and cofactors or by interfering with mRNA to alter expression at the translational level. The result is a network of changes that can change throughout an organism’s lifetime, altering the landscape as it interacts with the environment through lifestyle choices such as diet and exercise. These changes ultimately alter chromatin structure and affect stem cell biology. The interplay between lifestyle factors and epigenetic patterns in an increasingly aging population reveals the complex nature of ‘aging’ and how different epigenetic factors control MSC growth and function highlight something they are considering what to do.


According to the information theory of aging, the epigenetic landscape is lost as cells age. As a result, cellular identity is lost and cellular function is compromised. Dynamic changes in DNA methylation, hydroxymethylation, histone modifications, and non-coding RNA have been found in studies examining epigenetic changes in MSCs over time. These modifications lead to senescence, a unilateral differentiation that promotes adipogenesis at the expense of osteogenesis and heterochromatin loss. Mesenchymal stem cells have been compared to somatic cells to confirm their fitness and it is now recognized that chromatin structure is an important guardian of the genome and a transmitter of epigenetic information that changes with age increase. Interestingly, mesenchymal stem cells exhibit remarkably stable nucleosome positioning during senescence, and changes in stress response genes that ensure the establishment of defense mechanisms. MSC senescence is primarily driven by changes in chromatin structure and inhibition of stem genes due to reduced access to chromatin, especially along differentiation genes enriched in bivalent chromatin domains. Another level of research into potential therapeutic targets for combating stem cell aging and disease suggests that chromatin alterations appear to occur in regions where SNPs in various diseases such as obesity, immunity and bone disease have been identified. This is underscored by the finding that this finding highlights the utility of assessing chromatin accessibility. Chromatin structures and genomic regions associated with age-related increases in DNA methylation by MSCs in combination with H3K27me3 and H3K9me3 restricted histone markers are also thought to be important in osteoporosis, primarily histone and intervening DNA modifications. Affected by Specifically, Ezh2 has been shown to deactivate the antioxidant defense system, inhibit bone formation, and deposit H3K27me3 in bone-bound genes in MSCs generated from osteoporotic specimens.


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