Heme inhibits cartilage metabolism and growth in vitro

Vassilopoulou‐Sellin, Rena; Thompson, M.Malynn; Oyedeji, Caroline O.; Samaan, Naguib A.

doi:10.1016/0026-0495(89)90179-0

Cited by 3 publications

(1 citation statement)

References 26 publications

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“…It has been observed that hemoglobin, heme, and bilirubin have an inhibitory effect on cartilage metabolism and growth in vitro although the molecular mechanism is not clear [ 44 – 46 ]. FLVCR1 is expressed at high levels during development in the yolk sac and placenta [ 5 ].…”

Section: Diamond Blackfan Anemia As a Putative Disorder Of Heme Mementioning

confidence: 99%

Diamond Blackfan Anemia at the Crossroad between Ribosome Biogenesis and Heme Metabolism

Chiabrando

Tolosano

2010

Advances in Hematology

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Diamond-Blackfan anemia (DBA) is a rare, pure red-cell aplasia that presents during infancy. Approximately 40% of cases are associated with other congenital defects, particularly malformations of the upper limb or craniofacial region. Mutations in the gene coding for the ribosomal protein RPS19 have been identified in 25% of patients with DBA, with resulting impairment of 18S rRNA processing and 40S ribosomal subunit formation. Moreover, mutations in other ribosomal protein coding genes account for about 25% of other DBA cases. Recently, the analysis of mice from which the gene coding for the heme exporter Feline Leukemia Virus subgroup C Receptor (FLVCR1) is deleted suggested that this gene may be involved in the pathogenesis of DBA. FLVCR1-null mice show a phenotype resembling that of DBA patients, including erythroid failure and malformations. Interestingly, some DBA patients have disease linkage to chromosome 1q31, where FLVCR1 is mapped. Moreover, it has been reported that cells from DBA patients express alternatively spliced isoforms of FLVCR1 which encode non-functional proteins. Herein, we review the known roles of RPS19 and FLVCR1 in ribosome function and heme metabolism respectively, and discuss how the deficiency of a ribosomal protein or of a heme exporter may result in the same phenotype.

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Section: Diamond Blackfan Anemia As a Putative Disorder Of Heme Mementioning

confidence: 99%

Diamond Blackfan Anemia at the Crossroad between Ribosome Biogenesis and Heme Metabolism

Chiabrando

Tolosano

2010

Advances in Hematology

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Bilirubin as an inhibitor of cartilage metabolism: Effect on avian chondrocyte proliferation in cell culture

Vassilopoulou‐Sellin

Rey-Bear

Oyedeji

1990

Journal of Bone and Mineral Research

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Elevated levels of bilirubin and other tetrapyrroles are common to a number of chronic hematologic and liver diseases that can result in growth failure. This report establishes a cellular model system for the study of these endogenous growth inhibitors. Primary chondrocyte cultures were prepared from embryonic chick cartilage; cells were incubated (0.3 X 10(5) cells per plate) in tissue culture medium containing 10% fetal bovine serum (FBS) with or without added bilirubin, 0.01-0.10 mM. Bilirubin caused profound, dose-dependent inhibition of chondrocyte proliferation: after 7 days, control incubations contained 11.45 +/- 2.0 X 10(5) cells per plate versus 4.92 +/- 0.55 X 10(5) cells per plate for wells with added 0.01 mM bilirubin and 1.76 +/- 0.30 X 10(5) for cultures with added 0.05 mM bilirubin. In chondrocytes cultured for 3 days, the addition of 0.05 mM bilirubin was associated with inhibition of [3H]thymidine incorporation into DNA (47 +/- 5% of control), [3H]uridine incorporation into RNA (11 +/- 0.05% of control), and [14C]leucine incorporation into proteins (16 +/- 1% of control). The inhibition of chondrocyte proliferation induced by a range of bilirubin concentrations (0.01-0.10 mM) was in no way attenuated by the addition of physiologic concentrations of albumin (4 g/dl). After 3 days in media containing bilirubin or heme (at equimolar concentrations), chondrocytes were subsequently incubated in FBS alone for an additional 3 days; only partial reversal of the bilirubin (or heme)-induced inhibition was then observed.(ABSTRACT TRUNCATED AT 250 WORDS)

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Hematoporphyrin can inhibit the metabolism and growth of embryonic chicken cartilage in vitro

Vassilopoulou‐Sellin

Oyedeji

1990

Metabolism

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Heme inhibits cartilage metabolism and growth in vitro

Cited by 3 publications

References 26 publications

Diamond Blackfan Anemia at the Crossroad between Ribosome Biogenesis and Heme Metabolism

Diamond Blackfan Anemia at the Crossroad between Ribosome Biogenesis and Heme Metabolism

Bilirubin as an inhibitor of cartilage metabolism: Effect on avian chondrocyte proliferation in cell culture

Hematoporphyrin can inhibit the metabolism and growth of embryonic chicken cartilage in vitro

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