Localization of the expression of types I, III, and IV collagen, TGF-β1 and c-fos genes in developing human calvarial bones

Sandberg, M; Autio–Harmainen, Helena; Vuorio, Eero

doi:10.1016/0012-1606(88)90438-1

Cited by 99 publications

(37 citation statements)

References 31 publications

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“…The lack of Alcian blue staining in the other half of the calvarial pairs, which consist of similar cellular constituents but are cultured in a calcium rich environment, suggests that expression of the chondrogenic potential may not take place unless the cells are exposed to the appropriate environmental stimuli. It is known that cells of fetal rat and human calvaria are significantly heterogenous with respect to morphology (Wiestner et al, 1981;Puzas and Jensen, 1982;Sandberg et al, 19881, their al., 1982; Puzas and Jensen, 19821, and collagen biosynthesis and distribution (Wiestner et al, 1981;Aubin et al, 1982;Sandberg et al, 1988). For example, Bellows and Aubin (1989) identified only 0.3% of the cells in isolated rat calvarial populations as osteoprogenitor cells.…”

Section: Discussionmentioning

confidence: 99%

Chondrogenic potential of chick embryonic calvaria: I. Low calcium permits cartilage differentiation

Jacenko

Tuan

1995

Developmental Dynamics

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Calvaria from day-14 calciumdeficient chick embryos produced by long-term maintenance in shell-less culture, exhibit a cartilage-like phenotype (Jacenko and Tuan 119861 Dev. Biol. 11521L232), which is restored to an osteogenic phenotype upon calcium repletion to the embryo. The expression of cartilage markers in a typically osteogenic tissue under calcium deficiency implies the presence of chondrogenic cells, and questions the conditions associated with calcium deficiency which may cause their divergent pathway of differentiation. In the present study, by explanting normal and shell-less embryonic calvarial pairs in organ culture in vitro and experimentally regulating their calcium supply, the calcium status of the calvaria was modulated as a function of medium calcium. Histological and immunoblotting analyses demonstrated for the first time that calvaria possess cells which can form genuine cartilage. This chondrogenic potential is expressed only in a low-calcium environment, where cartilage forms in both normal and shellless calvarial pairs; their calcium-suplemented counterparts, however, develop as fully osteogenic tissues. Furthermore, chondrogenesis in both normal and shell-less calvaria indicates that the chondrogenic cells must be endogenous constituents of the calvaria, rather than being derived elsewhere in response to systemic calcium deficiency. Finally, the correlation between matrix under-calcification and cartilage expression in the embryonic calvarium suggests that calcium, perhaps in the form of matrix mineral, may modulate cell differentiation during skeletogenesis.

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Section: Discussionmentioning

confidence: 99%

Chondrogenic potential of chick embryonic calvaria: I. Low calcium permits cartilage differentiation

Jacenko

Tuan

1995

Developmental Dynamics

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“…Transcript levels of genes necessary for the growth, remodeling, and maintenance of the extracellular matrix in wound healing were highly expressed in wounds from both groups, suggesting their importance in the pathogenesis of HO. In addition, transcript levels of genes encoding type I collagen (COL1A1, COL1A2), the predominant structural component of bone, also were highly expressed in both groups [43]. Significant differences between the two cohorts, however, were found regarding systemic injury severity and the local inflammatory response to injury.…”

Section: Gene Upregulation In Patients Who Developed Heterotopic Ossimentioning

confidence: 95%

“…As seen in our study, the expression of transcripts necessary for synthesis of cartilaginous matrix (COL2A1, COL10A1, COL11A1, COMP) and tissue remodeling (MMP8, MMP9) were upregulated in wounds in which HO developed. Specifically, COL2A1 encodes type II collagen, the chief component of cartilaginous matrix, whereas COL10A1 encodes type X collagen, a marker for hypertrophic chondrocytes intimately associated with calcification of the cartilaginous matrix [40,43]. Transcript levels of genes necessary for the growth, remodeling, and maintenance of the extracellular matrix in wound healing were highly expressed in wounds from both groups, suggesting their importance in the pathogenesis of HO.…”

Section: Gene Upregulation In Patients Who Developed Heterotopic Ossimentioning

confidence: 99%

Osteogenic Gene Expression Correlates With Development of Heterotopic Ossification in War Wounds

Evans

Potter

Brown

et al. 2013

Clin Orthop Relat Res

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Background Heterotopic ossification (HO) is a frequent complication of modern wartime extremity injuries. The biological mechanisms responsible for the development of HO in traumatic wounds remain elusive. Question/purposes The aims of our study were to (1) characterize the expression profile of osteogenesis-related gene transcripts in traumatic war wounds in which HO developed; and (2) determine whether expression at the mRNA level correlated with functional protein expression and HO formation. Methods Biopsy specimens from 54 high-energy penetrating extremity wounds obtained at the initial and final surgical débridements were evaluated. The levels of selected osteogenic-related gene transcripts from RNA extracts were assessed by quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. As a result of its key role in osteogenesis, the concentration of BMP-2 in the effluent of 29 wounds also was determined. Conclusions Important differences exist in the osteogenic gene expression profile of wounds in which HO developed compared with wounds in which it did not develop. The upregulation of multiple osteogenesis-related gene transcripts indicates the presence of a proosteogenic environment necessary for ectopic bone formation in traumatic wounds.

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“…Our postulate is partly built upon the following findings. First, TGF-P is produced by the calvaria in situ (Sandberg et al, 1988;Heine et al, 1987) and as cultured cells (Centrella and Canalis, 19851, and is found abundantly in the mineralized bone matrix (Seyedin et al, 1987). Second, TGF-p is active in calvarial bone growth, since direct injection of TGFp l and TGF-P2 into the subperiosteal space induced growth (Noda and Camilliere, 1989;Joyce et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Effect of systemic calcium deficiency on the expression of transforming growth factor‐β in chick embryonic calvaria

Sato

Tuan

1992

Developmental Dynamics

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The developmental process of intramembranous ossification involves bone formation directly from mesenchymal differentiation without a cartilage intermediate. We have previously observed that systemic calcium deficiency in the developing chick embryo, produced by long-term shell-less culture, results in the appearance of chondrocyte-like cells in the calvarium, a parietal bone which normally develops via intramembranous ossification. This investigation aims to analyze the mechanism underlying this calcium deficiency-related, aberrant appearance of cartilage phenotype in the chick embryonic calvarium. In view of the reported involvement of transforming growth factor p (TGF-P) in osteogenesis and chondrogenesis, we have examined and compared here the expression of TGF-p in the chick embryonic calvaria of normal (in ovo development, NL), shell-less (SL), and calcium-supplemented SL (SL + Ca) embryos. TGF-f3 expression was analyzed at the mRNA level by blot and in situ cDNA hybridization, and at the protein level by immunohistochemistry and immunoblotting. The results presented here indicate that: 1) TGF-p is expressed in the chick embryonic calvarium by both periosteal cells and osteocytes, as revealed by in situ hybridization and immunohistochemistry; 2) TGF-P expression is significantly increased in SL calvarium compared to NL calvarium, at both protein and mRNA levels; 3) the number of TGF-f3 expressing cells increases in the SL calvarium, particularly along the central, subcambial core region of the bone; and 4) exogenous calcium repletion to the SL embryo affects the expression of TGF-P such that the pattern approaches that in the NL embryo. Taken together, these results indicate that altered TGF-f3 expression accompanies the aberrant appearance of cartilage phenotype caused by systemic calcium deficiency. We postulate that normal cellular differentiation along the osteogenic pathway during embryonic intramembranous ossification is crucially dependent on regulated TGF-0 expression. o 1992 Wiley-Liss, Inc.

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Localization of the expression of types I, III, and IV collagen, TGF-β1 and c-fos genes in developing human calvarial bones

Cited by 99 publications

References 31 publications

Chondrogenic potential of chick embryonic calvaria: I. Low calcium permits cartilage differentiation

Chondrogenic potential of chick embryonic calvaria: I. Low calcium permits cartilage differentiation

Osteogenic Gene Expression Correlates With Development of Heterotopic Ossification in War Wounds

Effect of systemic calcium deficiency on the expression of transforming growth factor‐β in chick embryonic calvaria

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