ArticleExperimental and therapeutic medicine2018
The inhibitory roles of Ihh downregulation on chondrocyte growth and differentiation.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Cell signaling and transcriptional regulation of osteoblast lineage commitment, differentiation, bone formation, and homeostasis.Cell discovery · 2024Review
- Glucocorticoid induced bone disorders in children: Research progress in treatment mechanisms.Frontiers in endocrinology · 2023Review
- Article
- Circular RNA circANAPC2 mediates the impairment of endochondral ossification by miR-874-3p/SMAD3 signalling pathway in idiopathic short stature.Journal of cellular and molecular medicine · 2021Article
- Article
- The value of the hedgehog signal in osteoblasts in fluoride-induced bone-tissue injury.Journal of orthopaedic surgery and research · 2021Article
- Blockade of TRPM7 Alleviates Chondrocyte Apoptosis and Articular Cartilage Damage in the Adjuvant Arthritis Rat Model Through Regulation of the Indian Hedgehog Signaling Pathway.Frontiers in pharmacology · 2021Article
- Hsa_circularRNA_0079201 suppresses chondrocyte proliferation and endochondral ossification by regulating the microRNA‑140‑3p/SMAD2 signaling pathway in idiopathic short stature.International journal of molecular medicine · 2020Article
- MicroRNA-1 promotes cartilage matrix synthesis and regulates chondrocyte differentiation via post-transcriptional suppression of Ihh expression.Molecular medicine reports · 2020Article
- MALDI-TOF-MS-based high throughput genotyping of mutations associated with body measurement traits in cattle.Mammalian genome : official journal of the International Mammalian Genome Society · 2020Article
- MicroRNA-30a regulates chondrogenic differentiation of human bone marrow-derived mesenchymal stem cells through targeting Sox9.Experimental and therapeutic medicine · 2019Article
Corrections and comments
- Expression of concern · 2025-08-13Author Unresponsive · Concerns/Issues about Data · Duplication of Data · Euphemisms for Duplication · Investigation by Journal/Publisher · Investigation by Third Party · · See also: https://pubpeer.com/publications/54B9D6B61F50FDCFBBF8B1CE6FD4FA
- Expression of concern
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proliferative rate of chondrocytes affects bone elongation. Chondrocyte hypertrophy is required for endochondral bone formation as chondrocytes secrete factors required for osteoblast differentiation and maturation. Previous studies have demonstrated that the Indian hedgehog (Ihh) signaling pathway is a key regulator of skeletal development and homeostasis. The aim of the present study was to investigate the function of Ihh in chondrocyte proliferation and differentiation, as well as the underlying mechanisms. Ihh was knocked down in mouse chondrocyte cells using short hairpin RNA. Chondrocyte apoptosis and cell cycle arrest were assessed using flow cytometry and the results indicated that knockdown of Ihh significantly inhibited cell growth (P<0.05) and increased apoptosis (P<0.001) compared with negative control cells. Downregulation of Ihh also resulted in cell cycle arrest at G1 to S phase in chondrocytes. It was also observed that knockdown of Ihh decreased alkaline phosphatase activity and mineral deposition of chondrocytes. The inhibitory roles of Ihh downregulation on chondrocyte growth and differentiation may be associated with the transforming growth factor-β/mothers against decapentaplegic and osteoprotegerin/receptor activator of nuclear factor κB ligand signaling pathway. The results of the present study suggest that chondrocyte-derived Ihh is essential for maintaining bone growth plates and that manipulation of Ihh expression or its signaling components may be a novel therapeutic technique for the treatment of skeletal diseases, including achondroplasia.
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