The N- and C-terminal domains of parathyroid hormone-related protein affect differently the osteogenic and adipogenic potential of human mesenchymal stem cells

Casado-Díaz, Antonio; Santiago-Mora, Raquel; Quesada, J. M.

doi:10.3858/emm.2010.42.2.010

Cited by 14 publications

(10 citation statements)

References 43 publications

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“…It might be possible that various fragments (N terminal and C terminal) of Parathyroid hormone-related peptide (PTHrP) are responsible for various activities. This is corroborated by the work of Casado-Díaz et al [ 10 ]. They showed that the N terminus was able to induce osteogenic differentiation, whereas the C terminus induced adipogenic differentiation of mesenchymal stem cells.…”

Section: Introductionsupporting

confidence: 82%

Parathyroid Hormone Secretion and Receptor Expression Determine the Age-Related Degree of Osteogenic Differentiation in Dental Pulp Stem Cells

Bhandi

Alkahtani

Reda

et al. 2021

JPM

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Objective: To demonstrate the levels of parathyroid hormone secretion and genetic expressions of parathyroid hormone (PTH) and PTH1 receptor (PTH1R) genes in the dental pulp stem cells (DPSCs) from different age groups before and after induction of osteogenic differentiation. In addition, we also wanted to check their correlation with the degree of osteogenic differentiation. Methods: Human primary DPSCs from three age groups (milk tooth (SHEDs), 7–12 years old; young DPSCs (yDPSCs), 20–40 years old; old DPSCs (oDPSCs), 60+ years old) were characterized for mesenchymal stem cell (MSC) markers. DPSCs were subjected to osteogenic differentiation and functional staining. Gene expression levels were analyzed by qRT-PCR. Surface receptor analysis was done by flow cytometry. Comparative protein levels were evaluated by ELISA. Results: All SHEDs, yDPSCs, and oDPSCs were found to be expressing mesenchymal stem cell markers. SHEDs showed more mineralization than yDPSCs and oDPSCs after osteogenic induction. SHEDs exhibited higher expression of PTH and PTH1R before and after osteogenic induction, and after osteogenic induction, SHEDs showed more expression for RUNX2, ALPL, and OCN. Higher levels of PTH were observed in SHEDs and yDPSCs, and the number of PTH1R positive cells was relatively lower in yDPSCs and oDPSCs than in SHEDs. After osteogenic induction, SHEDs were superior in the secretion of OPG, and the secretions of ALPL and PTH and the number of PTH1R positive cells were relatively low in the oDPSCs. Conclusions: The therapeutic quality of dental pulp stem cells is largely based on their ability to retain their stemness characteristics. This study emphasizes the criterion of aging, which affects the secretion of PTH by these cells, which in turn attenuates their osteogenic potential.

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Section: Introductionsupporting

confidence: 82%

Parathyroid Hormone Secretion and Receptor Expression Determine the Age-Related Degree of Osteogenic Differentiation in Dental Pulp Stem Cells

Bhandi

Alkahtani

Reda

et al. 2021

JPM

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“…Another study has shown that in 3T3-L1 cells, PTHrP mediates MAPK activation through the PKA pathway, thus also enhancing PPAR␥ activation (23). Moreover, our data and that of others have demonstrated that PTHrP expression was higher in undifferentiated stem cells and decreases until nondetectable levels in terminally differentiated cells (33). Consequently, it might be expected that the silencing of PTHrP could negatively regulate PPAR␥ activation and the expression of adipogenic genes, which may inhibit the final differentiation of preadipocytes into adipocytes.…”

Section: Discussionsupporting

confidence: 70%

Parathyroid Hormone-Related Protein, Human Adipose-Derived Stem Cells Adipogenic Capacity and Healthy Obesity

Roca-Rodriguez

Bekay

Garrido‐Sánchez

et al. 2015

The Journal of Clinical Endocrinology & Metabolism

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“…[ 26 ] Similarly, Parathyroid hormone related protein (1-36) (PTHrP(1-36)) has been shown to induce a mild osteogenic effect and inhibit adipocytic effect in human mesenchymal stem cell and thereby helping in osteoporosis beside its known action to modulate bone formation through promoting osteoblast differentiation. [ 27 ]…”

Section: Treatment Implication Of This Conceptmentioning

confidence: 99%

Obesity: Friend or foe for osteoporosis

Sharma¹,

Tandon²,

Mahajan³

et al. 2014

J Mid-life Health

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Osteoporosis and obesity are worldwide health problems. Interestingly, both are associated with significant morbidity and mortality. Both the diseases have common linkage as bone marrow mesenchymal stromal cells are the common precursors for both osteoblasts and adipocytes. Aging may shift composition of bone marrow by increasing adipocytes, osteoclast activity, and decreasing osteoblast activity, resulting into osteoporosis. Adipocytes secret leptin, adiponectin, adipsin, as well as proinflammatory cytokines, that contributes in pathogenesis of osteoporosis. This new concept supports the hypothesis, that the positive correlation of weight and body mass index (BMI) with bone mineral density (BMD) is not confirmed by large population-based studies. Thus, the previous concept, that obesity is protective for osteoporosis may not stand same as bone marrow fat deposition (adipogenesis) seen in obesity, is detrimental for bone health.

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The N- and C-terminal domains of parathyroid hormone-related protein affect differently the osteogenic and adipogenic potential of human mesenchymal stem cells

Abstract: Parathyroid hormone-related protein (PTHrP) is synthesized by diverse tissues, and its processing produces several fragments, each with apparently distinct autocrine and paracrine bioactivities.

Cited by 14 publications

References 43 publications

Parathyroid Hormone Secretion and Receptor Expression Determine the Age-Related Degree of Osteogenic Differentiation in Dental Pulp Stem Cells

Parathyroid Hormone Secretion and Receptor Expression Determine the Age-Related Degree of Osteogenic Differentiation in Dental Pulp Stem Cells

Parathyroid Hormone-Related Protein, Human Adipose-Derived Stem Cells Adipogenic Capacity and Healthy Obesity

Obesity: Friend or foe for osteoporosis

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