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International Journal of Molecular... Dec 2022Human adult mesenchymal stromal cells (MSCs) from a variety of sources may be used to repair defects in articular cartilage by inducing them into chondrogenic... (Review)
Review
Human adult mesenchymal stromal cells (MSCs) from a variety of sources may be used to repair defects in articular cartilage by inducing them into chondrogenic differentiation. The conditions in which optimal chondrogenic differentiation takes place are an area of interest in the field of tissue engineering. Chondrocytes exist in vivo in a normally hypoxic environment and thus it has been suggested that exposing MSCs to hypoxia may also contribute to a beneficial effect on their differentiation. There are two main stages in which MSCs can be exposed to hypoxia, the expansion phase when cells are cultured, and the differentiation phase when cells are induced with a chondrogenic medium. This systematic review sought to explore the effect of hypoxia at these two stages on human adult MSC chondrogenesis in vitro. A literature search was performed on PubMed, EMBASE, Medline via Ovid, and Cochrane, and 24 studies were ultimately included. The majority of these studies showed that hypoxia during the expansion phase or the differentiation phase enhances at least some markers of chondrogenic differentiation in adult MSCs. These results were not always demonstrated at the protein level and there were also conflicting reports. Studies evaluating continuous exposure to hypoxia during the expansion and differentiation phases also had mixed results. These inconsistent results can be explained by the heterogeneity of studies, including factors such as different sources of MSCs used, donor variability, level of hypoxia used in each study, time exposed to hypoxia, and differences in culture methodology.
Topics: Humans; Adult; Cells, Cultured; Chondrogenesis; Mesenchymal Stem Cells; Cell Differentiation; Chondrocytes; Hypoxia; Cell Hypoxia
PubMed: 36499531
DOI: 10.3390/ijms232315210 -
Nutrients Nov 2022Osteoporosis is caused by the deterioration of bone density and microstructure, resulting in increased fracture risk. It transpires due to an imbalanced skeletal... (Review)
Review
BACKGROUND
Osteoporosis is caused by the deterioration of bone density and microstructure, resulting in increased fracture risk. It transpires due to an imbalanced skeletal remodelling process favouring bone resorption. Various natural compounds can positively influence the skeletal remodelling process, of which naringenin is a candidate. Naringenin is an anti-inflammatory and antioxidant compound found in citrus fruits and grapefruit. This systematic review aims to present an overview of the available evidence on the skeletal protective effects of naringenin.
METHOD
A systematic literature search was conducted using the PubMed and Scopus databases in August 2022. Original research articles using cells, animals, or humans to investigate the bone protective effects of naringenin were included.
RESULTS
Sixteen eligible articles were included in this review. The existing evidence suggested that naringenin enhanced osteoblastogenesis and bone formation through BMP-2/p38MAPK/Runx2/Osx, SDF-1/CXCR4, and PI3K/Akt/-Fos/-Jun/AP-1 signalling pathways. Naringenin also inhibited osteoclastogenesis and bone resorption by inhibiting inflammation and the RANKL pathway.
CONCLUSIONS
Naringenin enhances bone formation while suppressing bone resorption, thus achieving its skeletal protective effects. It could be incorporated into the diet through fruit intake or supplements to prevent bone loss.
Topics: Humans; Animals; Phosphatidylinositol 3-Kinases; Flavanones; Osteogenesis; Bone Resorption
PubMed: 36432535
DOI: 10.3390/nu14224851 -
Nutrients Oct 2022The non-classical role of vitamin D has been investigated in recent decades. One of which is related to its role in skeletal muscle. Satellite cells are skeletal muscle... (Review)
Review
The non-classical role of vitamin D has been investigated in recent decades. One of which is related to its role in skeletal muscle. Satellite cells are skeletal muscle stem cells that play a pivotal role in skeletal muscle growth and regeneration. This systematic review aims to investigate the effect of vitamin D on satellite cells. A systematic search was performed in Scopus, MEDLINE, and Google Scholar. In vivo studies assessing the effect of vitamin D on satellite cells, published in English in the last ten years were included. Thirteen in vivo studies were analyzed in this review. Vitamin D increases the proliferation of satellite cells in the early life period. In acute muscle injury, vitamin D deficiency reduces satellite cells differentiation. However, administering high doses of vitamin D impairs skeletal muscle regeneration. Vitamin D may maintain satellite cell quiescence and prevent spontaneous differentiation in aging. Supplementation of vitamin D ameliorates decreased satellite cells' function in chronic disease. Overall, evidence suggests that vitamin D affects satellite cells' function in maintaining skeletal muscle homeostasis. Further research is needed to determine the most appropriate dose of vitamin D supplementation in a specific condition for the optimum satellite cells' function.
Topics: Satellite Cells, Skeletal Muscle; Vitamin D; Regeneration; Muscle Development; Muscle Fibers, Skeletal; Cell Differentiation; Muscle, Skeletal; Vitamins
PubMed: 36364820
DOI: 10.3390/nu14214558 -
Frontiers in Plant Science 2022Culture in temporary immersion systems (TIS) is a valuable tool for the semi-automation of high frequency somatic embryogenesis of coffee. This system allows the...
Culture in temporary immersion systems (TIS) is a valuable tool for the semi-automation of high frequency somatic embryogenesis of coffee. This system allows the intermittent exposure of explants to liquid medium in cycles of specific frequency and duration of immersion with renewal of the culture atmosphere in each cycle. TIS have revolutionized somatic embryogenesis of coffee plants as an alternative for scaling up and reducing costs associated with labor-intensive solid media culture. In Central America, somatic embryogenesis is employed on a commercial scale to produce F1 hybrids. In Asia and Africa, somatic embryogenesis is used for the multiplication of selected genotypes of and . Somatic embryogenesis of coffee plants is considered a model system for woody species due to its biological versatility and low frequency of somaclonal variation. Nevertheless, the success of somatic embryogenesis for mass propagation of coffee plants depends on the development, optimization, and transfer of complementary technologies. Temporary immersion using the RITA bioreactor is, so far, the best complementary tool for somatic embryogenesis of Arabica coffee for a single recipient with simple changes in liquid media. Likewise, high volume bioreactors, such as 10-L glass BIT and 10-L flexible disposable plastic bags, have been successfully used for somatic embryogenesis of other coffee species. These bioreactors allow the manipulation of thousands of embryos under semi-automated conditions. The protocols, advantages, and benefits of this technology have been well documented for organogenesis and somatic embryogenesis pathways. However, adaptation in commercial laboratories requires technical and logistical adjustments based on the biological response of the cultures as well as the costs of implementation and production. This review presents the historical and present background of TIS and its commercial application and, in particular, pertinent information regarding temporary immersion culture for somatic embryogenesis. The main limitations of this technology, such as hyperhydricity, asynchrony, and developmental abnormalities, are examined, and a critical analysis of current knowledge regarding physiological, biochemical, and molecular aspects of the plant response to temporary immersion is offered. Further, perspectives are provided for understanding and solving the morpho-physiological problems associated with temporary immersion culture of coffee plants. Systematic Review Registration.
PubMed: 36275513
DOI: 10.3389/fpls.2022.994578 -
Molecules (Basel, Switzerland) Aug 2022Hydroxyapatite (HA) is a well-known calcium phosphate ingredient comparable to human bone tissue. HA has exciting applications in many fields, especially biomedical... (Review)
Review
Hydroxyapatite (HA) is a well-known calcium phosphate ingredient comparable to human bone tissue. HA has exciting applications in many fields, especially biomedical applications, such as drug delivery, osteogenesis, and dental implants. Unfortunately, hydroxyapatite-based nanomaterials are synthesized by conventional methods using reagents that are not environmentally friendly and are expensive. Therefore, extensive efforts have been made to establish a simple, efficient, and green method to form nano-hydroxyapatite (NHA) biofunctional materials with significant biocompatibility, bioactivity, and mechanical strength. Several types of biowaste have proven to be a source of calcium in forming HA, including using chicken eggshells, fish bones, and beef bones. This systematic literature review discusses the possibility of replacing synthetic chemical reagents, synthetic pathways, and toxic capping agents with a green template to synthesize NHA. This review also shed insight on the simple green manufacture of NHA with controlled shape and size.
Topics: Animals; Bone and Bones; Cattle; Drug Delivery Systems; Durapatite; Humans; Nanostructures; Osteogenesis
PubMed: 36080349
DOI: 10.3390/molecules27175586 -
Biology of Sex Differences Jun 2022In this systematic review, we highlight the differences between the male and female zebrafish brains to understand their differentiation and their use in studying... (Review)
Review
In this systematic review, we highlight the differences between the male and female zebrafish brains to understand their differentiation and their use in studying sex-specific neurological diseases. Male and female brains display subtle differences at the cellular level which may be important in driving sex-specific signaling. Sex differences in the brain have been observed in humans as well as in non-human species. However, the molecular mechanisms of brain sex differentiation remain unclear. The classical model of brain sex differentiation suggests that the steroid hormones derived from the gonads are the primary determinants in establishing male and female neural networks. Recent studies indicate that the developing brain shows sex-specific differences in gene expression prior to gonadal hormone action. Hence, genetic differences may also be responsible for differentiating the brain into male and female types. Understanding the signaling mechanisms involved in brain sex differentiation could help further elucidate the sex-specific incidences of certain neurological diseases. The zebrafish model could be appropriate for enhancing our understanding of brain sex differentiation and the signaling involved in neurological diseases. Zebrafish brains show sex-specific differences at the hormonal level, and recent advances in RNA sequencing have highlighted critical sex-specific differences at the transcript level. The differences are also evident at the cellular and metabolite levels, which could be important in organizing sex-specific neuronal signaling. Furthermore, in addition to having one ortholog for 70% of the human gene, zebrafish also shares brain structural similarities with other higher eukaryotes, including mammals. Hence, deciphering brain sex differentiation in zebrafish will help further enhance the diagnostic and pharmacological intervention of neurological diseases.
Topics: Animals; Brain; Female; Gonads; Male; Mammals; Sex Characteristics; Sex Differentiation; Zebrafish
PubMed: 35715828
DOI: 10.1186/s13293-022-00442-2 -
Scientific Reports Jun 2022Focal chondral defects of the knee are common and their management is challenging. This study investigated the efficacy and safety of Autologous Matrix-Induced... (Meta-Analysis)
Meta-Analysis
Focal chondral defects of the knee are common and their management is challenging. This study investigated the efficacy and safety of Autologous Matrix-Induced Chondrogenesis (AMIC) for focal chondral defects of the knee. A systematic review and meta-analysis was conducted (according to the 2020 PRISMA statement) to investigate the efficacy of AMIC in improving symptoms and to compare AMIC versus microfracture (MFx). In January 2022, the following databases were accessed: Pubmed, Web of Science, Google Scholar, Embase. No time constrain was used for the search. All the clinical trials investigating AMIC and/or those comparing AMIC versus MFx for focal chondral defects of the knee were accessed. Only studies published in peer reviewed journals were considered. Studies which investigated other locations of the defects rather than knee were not eligible, nor those reporting data form mixed locations. Studies which reported data on revision settings, as well as those investigating efficacy on kissing lesions or multiple locations, were not suitable. The mean difference (MD) and odd ratio (OR) effect measure were used for continuous and binary data, respectively. Data from 18 studies (548 patients) were retrieved with a mean follow-up of 39.9 ± 26.5 months. The mean defect size was 3.2 ± 1.0 cm. The visual analogue scale (VAS) decreased of - 3.9/10 (95% confidence interval (CI) - 4.0874 to -3.7126), the Tegner Activity Scale increased of + 0.8/10 (95% CI 0.6595 to 0.9405). The Lysholm Knee Scoring System increased of + 28.9/100 (95% CI 26.8716 to 29.1284), as did the International Knee Documentation Committee (IKDC) + 33.6/100 (95% CI 32.5800 to 34.6200). At last follow-up no patient showed signs of hypertrophy. 4.3% (9 of 210) of patients underwent revision procedures. The rate of failure was 3.8% (9 of 236). Compared to MFx, AMIC demonstrated lower VAS score (MD: - 1.01; 95% CI - 1.97 to 0.05), greater IKDC (MD: 11.80; 95% CI 6.65 to 16.94), and lower rate of revision (OR: 0.16; 95% CI 0.06 to 0.44). AMIC is effective for focal chondral defects of the knee. Furthermore, AMIC evidenced greater IKDC, along with a lower value of VAS and rate of revision compared to MFx.
Topics: Cartilage Diseases; Cartilage, Articular; Chondrogenesis; Humans; Knee Joint; Transplantation, Autologous
PubMed: 35661147
DOI: 10.1038/s41598-022-13591-6 -
Behavioral and Brain Functions : BBF May 2022Genetic variants of DCX, COMT and FMR1 have been linked to neurodevelopmental disorders related to intellectual disability and social behavior. In this systematic review... (Review)
Review
Genetic variants of DCX, COMT and FMR1 have been linked to neurodevelopmental disorders related to intellectual disability and social behavior. In this systematic review we examine the roles of the DCX, COMT and FMR1 genes in the context of hippocampal neurogenesis with respect to these disorders with the aim of identifying important hubs and signaling pathways that may bridge these conditions. Taken together our findings indicate that factors connecting DCX, COMT, and FMR1 in intellectual disability and social behavior may converge at Wnt signaling, neuron migration, and axon and dendrite morphogenesis. Data derived from genomic research has identified a multitude of genes that are linked to brain disorders and developmental differences. Information about where and how these genes function and cooperate is lagging behind. The approach used here may help to shed light on the biological underpinnings in which key genes interface and may prove useful for the testing of specific hypotheses.
Topics: Catechol O-Methyltransferase; Cognitive Dysfunction; Fragile X Mental Retardation Protein; Hippocampus; Humans; Intellectual Disability; Neurogenesis; Social Behavior
PubMed: 35590332
DOI: 10.1186/s12993-022-00191-7 -
World Journal of Surgical Oncology May 2022Glioblastoma is one of the most aggressive tumors. The etiology and the factors determining its onset are not yet entirely known. This study investigates the origins of...
BACKGROUND
Glioblastoma is one of the most aggressive tumors. The etiology and the factors determining its onset are not yet entirely known. This study investigates the origins of GBM, and for this purpose, it focuses primarily on developmental gliogenic processes. It also focuses on the impact of the related neurogenic developmental processes in glioblastoma oncogenesis. It also addresses why glial cells are at more risk of tumor development compared to neurons.
METHODS
Databases including PubMed, MEDLINE, and Google Scholar were searched for published articles without any date restrictions, involving glioblastoma, gliogenesis, neurogenesis, stemness, neural stem cells, gliogenic signaling and pathways, neurogenic signaling and pathways, and astrocytogenic genes.
RESULTS
The origin of GBM is dependent on dysregulation in multiple genes and pathways that accumulatively converge the cells towards oncogenesis. There are multiple layers of steps in glioblastoma oncogenesis including the failure of cell fate-specific genes to keep the cells differentiated in their specific cell types such as p300, BMP, HOPX, and NRSF/REST. There are genes and signaling pathways that are involved in differentiation and also contribute to GBM such as FGFR3, JAK-STAT, and hey1. The genes that contribute to differentiation processes but also contribute to stemness in GBM include notch, Sox9, Sox4, c-myc gene overrides p300, and then GFAP, leading to upregulation of nestin, SHH, NF-κB, and others. GBM mutations pathologically impact the cell circuitry such as the interaction between Sox2 and JAK-STAT pathway, resulting in GBM development and progression.
CONCLUSION
Glioblastoma originates when the gene expression of key gliogenic genes and signaling pathways become dysregulated. This study identifies key gliogenic genes having the ability to control oncogenesis in glioblastoma cells, including p300, BMP, PAX6, HOPX, NRSF/REST, LIF, and TGF beta. It also identifies key neurogenic genes having the ability to control oncogenesis including PAX6, neurogenins including Ngn1, NeuroD1, NeuroD4, Numb, NKX6-1 Ebf, Myt1, and ASCL1. This study also postulates how aging contributes to the onset of glioblastoma by dysregulating the gene expression of NF-κB, REST/NRSF, ERK, AKT, EGFR, and others.
Topics: Brain Neoplasms; Carcinogenesis; Cell Line, Tumor; Gene Expression Regulation, Neoplastic; Glioblastoma; Humans; Janus Kinases; NF-kappa B; Neoplastic Stem Cells; Neurogenesis; SOXC Transcription Factors; STAT Transcription Factors; Signal Transduction
PubMed: 35538578
DOI: 10.1186/s12957-022-02602-5 -
Frontiers in Immunology 2022In most patients with aplastic anemia (AA), the diagnosis is limited to a description of the symptoms. Lack of understanding of the underlying pathophysiological...
BACKGROUND
In most patients with aplastic anemia (AA), the diagnosis is limited to a description of the symptoms. Lack of understanding of the underlying pathophysiological mechanisms causing bone marrow failure (BMF), hampers tailored treatment. In these patients, auto-immune cell-mediated destruction of the bone marrow is often presumed to be the causative mechanism. The status of the bone marrow microenvironment, particularly the mesenchymal stromal cell (MSC) component, was recently suggested as a potential player in the pathophysiology of AA. Therefore, functional, and immune modulatory characteristics of bone marrow MSCs might represent important parameters for AA.
OBJECTIVE
To conduct a systematic review to evaluate functional properties of MSCs derived from patients with AA compared to healthy controls.
METHODS
According to PRISMA guidelines, a comprehensive search strategy was performed by using online databases (Pubmed, ISI Web of Science, Embase, and the Cochrane Library). Studies reporting on phenotypical characterization, proliferation potential, differentiation capacity, immunomodulatory potential, and ability to support hematopoiesis were identified and screened using the Rayyan software tool.
RESULTS
23 articles were included in this systematic review, describing a total of 324 patients with AA and 285 controls. None of the studies identified a significant difference in expression of any MSC surface marker between both groups. However, AA-MSCs showed a decreased proliferation potential, an increased tendency to differentiate into the adipogenic lineage and decreased propensity towards osteogenic differentiation. Importantly, AA-MSCs show reduced capacity of immunosuppression and hematopoietic support in comparison to healthy controls.
CONCLUSION
We conclude that there are indications for a contribution of MSCs in the pathophysiology of AA. However, the current evidence is of poor quality and requires better defined study populations in addition to a more robust methodology to study MSC biology at a cellular and molecular level. Future studies on bone marrow microenvironment should aim at elucidating the interaction between MSCs, hematopoietic stem cells (HSCs) and immune cells to identify impairments associated with/causing BMF in patients with AA.
Topics: Anemia, Aplastic; Bone Marrow; Cell Differentiation; Humans; Mesenchymal Stem Cells; Osteogenesis
PubMed: 35355996
DOI: 10.3389/fimmu.2022.859668