Erratum: Alkaline Phosphatase Controls Lineage Switching of Mesenchymal Stem Cells by Regulating the LRP6/GSK3β Complex in Hypophosphatasia: Erratum.

[This corrects the article DOI: 10.7150/thno.27372.

Synthesis of Diaryl Ethers via Hypervalent Iodine-Mediated C-H Functionalization.

A hypervalent iodine-reagent-based C-H functionalization strategy was utilized to synthesize diaryl ethers. This method directly transforms various arenes into their corresponding diaryliodonium salts, followed by a C-O coupling reaction to produce structurally diverse diaryl ethers. The efficacy of this approach in the late-stage structural modifications of complex molecules was demonstrated.

A Senescence-Associated Secretory Phenotype of Bone Marrow Mesenchymal Stem Cells Inhibits the Viability of Breast Cancer Cells.

Breast cancer, the most prevalent malignancy in women, often progresses to bone metastases, especially in older individuals. Dormancy, a critical aspect of bone-metastasized breast cancer cells (BCCs), enables them to evade treatment and recur. This dormant state is regulated by bone marrow mesenchymal stem cells (BMMSCs) through the secretion of various factors, including those associated with senescence.

General requirements for the production of extracellular vesicles derived from human stem cells.

'General requirements for the production of extracellular vesicles derived from human stem cells' is the first guideline for stem cells derived extracellular vesicles in China, jointly drafted and agreed upon by experts from the Chinese Society for Stem Cell Research. This standard specifies the general requirements, process requirements, packaging and labelling requirements and storage requirements for preparing extracellular vesicles derived from human stem cells, which is applicable to the research and production of extracellular vesicles derived from stem cells. It was originally released by the China Society for Cell Biology on 30 August 2022.

Targeted inhibition of osteoclastogenesis reveals the pathogenesis and therapeutics of bone loss under sympathetic neurostress.

Sympathetic cues via the adrenergic signaling critically regulate bone homeostasis and contribute to neurostress-induced bone loss, but the mechanisms and therapeutics remain incompletely elucidated. Here, we reveal an osteoclastogenesis-centered functionally important osteopenic pathogenesis under sympatho-adrenergic activation with characterized microRNA response and efficient therapeutics. We discovered that osteoclastic miR-21 was tightly regulated by sympatho-adrenergic cues downstream the β2-adrenergic receptor (βAR) signaling, critically modulated osteoclastogenesis in vivo by inhibiting programmed cell death 4 (Pdcd4), and mediated detrimental effects of both isoproterenol (ISO) and chronic variable stress (CVS) on bone.

Erratum: Resveratrol counteracts bone loss via mitofilin-mediated osteogenic improvement of mesenchymal stem cells in senescence-accelerated mice: Erratum.

[This corrects the article DOI: 10.7150/thno.23620.

Erratum to "Gli1+ Cells Residing in Bone Sutures Respond to Mechanical Force via IP3R to Mediate Osteogenesis".

[This corrects the article DOI: 10.1155/2021/8138374.].

Sympathetic Neurostress Drives Osteoblastic Exosomal MiR-21 Transfer to Disrupt Bone Homeostasis and Promote Osteopenia.

Innervation and extracellular vesicle secretion co-exist in the local tissue microenvironment for message transfer, but whether they are interconnected to regulate organ homeostasis remains unknown. Sympatho-adrenergic activation is implicated in stress-induced depression and leads to bone loss, but the mechanisms and therapeutics are incompletely elucidated. Here, it is revealed that sympathetic neurostress through the β -adrenergic receptor (β1/2-AR) signaling triggers the transcription response of a microRNA, miR-21, in osteoblasts, which is transferred to osteoclast progenitors via exosomes for dictating osteoclastogenesis.

Gli1 Cells Residing in Bone Sutures Respond to Mechanical Force via IPR to Mediate Osteogenesis.

Early orthodontic correction of skeletal malocclusion takes advantage of mechanical force to stimulate unclosed suture remodeling and to promote bone reconstruction; however, the underlying mechanisms remain largely unclear. Gli1 cells in maxillofacial sutures have been shown to participate in maxillofacial bone development and damage repair. Nevertheless, it remains to be investigated whether these cells participate in mechanical force-induced bone remodeling during orthodontic treatment of skeletal malocclusion.

Glycemic control by umbilical cord-derived mesenchymal stem cells promotes effects of fasting-mimicking diet on type 2 diabetic mice.

Background: Hepatic steatosis is a big hurdle to treat type 2 diabetes (T2D). Fasting-mimicking diet (FMD) has been shown to be an effective intervention in dyslipidemia of T2D. However, fasting may impair the normal glucose metabolism.

Mesenchymal stromal cell-mediated immune regulation: A promising remedy in the therapy of type 2 diabetes mellitus.

Type 2 diabetes mellitus (T2DM) is a major threat to global public health, with increasing prevalence as well as high morbidity and mortality, to which immune dysfunction has been recognized as a crucial contributor. Mesenchymal stromal cells (MSCs), obtained from various sources and possessing potent immunomodulatory abilities, have displayed great therapeutic potential for T2DM. Interestingly, the immunomodulatory capabilities of MSCs are endowed and plastic.

Correction: prevents bone ageing sensitivity by specifically regulating senescence and differentiation in mesenchymal stem cells.

[This corrects the article DOI: 10.1038/s41413-018-0029-4.].

Gli1 Cells Couple with Type H Vessels and Are Required for Type H Vessel Formation.

Mesenchymal stem/stromal cells (MSCs) reside in the perivascular niche and modulate tissue/organ homeostasis; however, little is known about whether and how their localization and function are linked. Particularly, whether specific MSC subsets couple with and regulate specialized vessel subtypes is unclear. Here, we show that Gli1 cells, which are a subpopulation of MSCs couple with and regulate a specialized form of vasculature.

Mechanosensing by Gli1 cells contributes to the orthodontic force-induced bone remodelling.

Objectives: Gli1 cells have received extensive attention in tissue homeostasis and injury mobilization. The aim of this study was to investigate whether Gli1 cells respond to force and contribute to bone remodelling.

Materials And Methods: We established orthodontic tooth movement (OTM) model to assess the bone response for mechanical force.

Ionomycin ameliorates hypophosphatasia via rescuing alkaline phosphatase deficiency-mediated L-type Ca channel internalization in mesenchymal stem cells.

The loss-of-function mutations in the ALPL result in hypophosphatasia (HPP), an inborn metabolic disorder that causes skeletal mineralization defects. In adults, the main clinical features are early loss of primary or secondary teeth, osteoporosis, bone pain, chondrocalcinosis, and fractures. However, guidelines for the treatment of adults with HPP are not available.

Epigenetic Regulation of Mesenchymal Stem Cell Homeostasis.

Mesenchymal stem cells (MSCs) have putative roles in maintaining adult tissue health, and the functional decline of MSCs has emerged as a crucial pathophysiological driver of various diseases. Epigenetic regulation is essential for establishing and preserving MSC homeostasis in vivo. Furthermore, growing evidence suggests that epigenetic dysregulation contributes to age- and disease-associated MSC alterations.

Mitochondrial Regulation of Stem Cells in Bone Homeostasis.

Mitochondria have emerged as key contributors to the organismal homeostasis, in which mitochondrial regulation of stem cells is becoming increasingly important. Originated from mesenchymal stem cell (MSC) and hematopoietic stem cell (HSC) lineage commitments and interactions, bone is a representative organ where the mitochondrial essentiality to stem cell function has most recently been discovered, underlying skeletal health, aging, and diseases. Furthermore, mitochondrial medications based on modulating stem cell specification are emerging to provide promising therapies to counteract bone aging and pathologies.

Gender-independent efficacy of mesenchymal stem cell therapy in sex hormone-deficient bone loss via immunosuppression and resident stem cell recovery.

Osteoporosis develops with high prevalence in both postmenopausal women and hypogonadal men. Osteoporosis results in significant morbidity, but no cure has been established. Mesenchymal stem cells (MSCs) critically contribute to bone homeostasis and possess potent immunomodulatory/anti-inflammatory capability.

Alkaline Phosphatase Controls Lineage Switching of Mesenchymal Stem Cells by Regulating the LRP6/GSK3β Complex in Hypophosphatasia.

Lineage differentiation of bone marrow mesenchymal stem cells (BMMSCs) is the key to bone-fat reciprocity in bone marrow. To date, the regulators of BMMSC lineage switching have all been identified to be transcription factors, and researchers have not determined whether other genes control this process. This study aims to reveal a previously unknown role of tissue-nonspecific alkaline phosphatase (TNSALP) in controlling BMMSC lineage selection.

NDRG2 suppression as a molecular hallmark of photoreceptor-specific cell death in the mouse retina.

Photoreceptor cell death is recognized as the key pathogenesis of retinal degeneration, but the molecular basis underlying photoreceptor-specific cell loss in retinal damaging conditions is virtually unknown. The N-myc downstream regulated gene (NDRG) family has recently been reported to regulate cell viability, in particular NDRG1 has been uncovered expression in photoreceptor cells. Accordingly, we herein examined the potential roles of NDRGs in mediating photoreceptor-specific cell loss in retinal damages.

prevents bone ageing sensitivity by specifically regulating senescence and differentiation in mesenchymal stem cells.

Mutations in the liver/bone/kidney alkaline phosphatase () gene cause hypophosphatasia (HPP) and early-onset bone dysplasia, suggesting that this gene is a key factor in human bone development. However, how and where acts in bone ageing is largely unknown. Here, we determined that ablation of induces prototypical premature bone ageing characteristics, including bone mass loss and marrow fat gain coupled with elevated expression of p16 (p16) and p53 due to senescence and impaired differentiation in mesenchymal stem cells (MSCs).

Reconstruction of Regenerative Stem Cell Niche by Cell Aggregate Engineering.

The niche plays critical roles in regulating functionality and determining regenerative outcomes of stem cells, for which establishment of favorable microenvironments is in demand in translational medicine. In recent years, the cell aggregate technology has shown immense potential to reconstruct a beneficial topical niche for stem cell-mediated regeneration, which has been recognized as a promising concept for high-density stem cell delivery with preservation of the self-produced, tissue-specific extracellular matrix microenvironments. Here, we describe the basic methodology of stem cell aggregate-based niche engineering and quality check indexes prior to application.

Deciduous autologous tooth stem cells regenerate dental pulp after implantation into injured teeth.

Pulp necrosis arrests root development in injured immature permanent teeth, which may result in tooth loss. However, dental pulp regeneration and promotion of root development remains challenging. We show that implantation of autologous tooth stem cells from deciduous teeth regenerated dental pulp with an odontoblast layer, blood vessels, and nerves in two animal models.