Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0265264 (HOS)
 1,119 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inflammatory cytokines like interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) are linked to abnormal cartilage and bone loss in a variety of pathological conditions. We have investigated the effect of TNF-alpha on the synthesis and/or steady-state mRNA levels of collagen, alkaline phosphatase (ALP), plasminogen activators (PAs) and their inhibitor PAI-1, and collagenases (MMPs) and their inhibitor TIMP-1 by human osteoblastic, HOS TE85, cells in monolayer cultures. HOS TE85 cells possess approximately 2000 TNF-alpha receptors per cell with a Kd value of 0.67 nM and receptor of approximately 60 kDa. TNF-alpha enhances urokinase-plasminogen activator (u-PA) activity and steady-state mRNA levels twofold without affecting tissue-plasminogen activator (t-PA) or PAI-1. The increase in u-PA mRNA is due to enhanced transcription of this gene. mRNA levels or activities of collagenase 1 (MMP-1), 72- and 92-kDa gelatinases (MMP-2 and MMP-9) are also nearly doubled with little change in the level of expression of TIMP-1. TNF-alpha does not significantly affect the activity or mRNA levels of ALP. TNF-alpha decreases collagen as well as general protein synthesis. However, the steady-state mRNA for the alpha 2 chain of collagen type I is increased three- to fourfold. These results show that TNF-alpha may increase pathological bone turnover by enhancing the rate of transcription of proteases capable of degrading the nonmineralized osteoid layer and decelerating the maturation of the extracellular matrix formed by osteoblasts.
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PMID:Modulation of proteases and their inhibitors in immortal human osteoblast-like cells by tumor necrosis factor-alpha in vitro. 808 23

Expression of progesterone receptors (PR) was studied in human osteoblast-like cell lines and primary human osteoblast cultures at the molecular level. Using the sensitive reverse transcriptase polymerase chain reaction (RT-PCR) and oligonucleotide primers which flank the progesterone-binding domain of human PR, progesterone receptor (PR) mRNA was detected in three osteoblast-like cell lines--HOS-TE85, MG-63, and SAOS-2. When compared with beta-actin gene expression, levels of PRmRNA transcripts varied between cell lines (PRmRNA in HOS-TE85 > MG-63 >> SAOS-2). In addition, RT-PCR confirmed the presence of PRmRNA transcripts in primary human osteoblast cells cultured from collagenase-treated bone. Immunostaining was used to visualize PR protein in cells. All osteoblast-like cell lines showed specific staining for PR. Immunoreactivity was distributed equally in the nucleus and cytoplasm. The level of staining was significantly lower than that detected in PR-positive MCF-7 breast cancer cells though well above background levels obtained for PR-negative HeLa cells. The finding that PR is expressed at both the level of mRNA and protein in several osteoblast-like cell lines as well as in human primary osteoblast cultures indicates that bone-forming osteoblast cells are direct targets for progesterone action.
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PMID:Progesterone receptors are expressed in human osteoblast-like cell lines and in primary human osteoblast cultures. 858 76

Matrix degrading enzymes released upon autocrine and/or paracrine induction exert a key role in modulating tumor cell behavior. Osteosarcoma is a highly metastatic cancer, with a redundancy of autocrine loops. Here we report that human osteosarcoma cells express a wide array of chemokine receptors and respond to chemokine activation with the release of N-acetyl-beta-D-glucosaminidase and gelatinase/collagenase activity. Of the two cell lines studied, the osteoblast-like MG-63 showed a higher responsivity compared to the less differentiated HOS. This suggests that chemokine modulation of matrix degrading enzymes requires the maintaining of the osteoblastic phenotype and of signaling pathways which occur in normal tissue.
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PMID:Human osteosarcoma cells release matrix degrading enzymes in response to chemokine activation. 1111 33

Acute ultraviolet (UV)-B irradiation causes skin wrinkle formation associated with hyperplasia of cutaneous blood vessels. This study reports that increased dermal oxygen tension attenuates acute UVB-induced angiogenesis and wrinkle formation. Twenty-four hairless mice (HOS:HR-1) were assigned to 3 groups: 1) control group, 2) UVB-irradiated (UVB) group, and 3) UVB-irradiated and hyperoxia-exposed (UVB+HO) group. The backs of the mice were exposed to UVB irradiation 3 times per week for a 5-wk period. To increase dermal oxygen tension, the mice were exposed to hyperoxia (90% oxygen) for 2 h immediately after each UVB irradiation. Hyperoxic exposure increased dermal oxygen tension by about 10 times compared with the control level. Degree of wrinkle formation and epidermal thickness increased significantly after a 5-wk UVB-irradiation period, whereas hyperoxic exposure attenuated these increases. Tissue adenosine triphosphate concentration and angiogenesis increased significantly only in the UVB group compared with the control group. Although the expression of hypoxia inducible factor-1alpha mRNA, a key molecule for angiogenesis, increased significantly in the UVB and UVB+HO groups compared with the control group, the protein level increased significantly only in the UVB group. The activity of matrix metalloproteinase-2 and -9, critical molecules for angiogenesis, did not increase in the UVB and UVB+HO groups compared with the control group. Active type 1 collagenase activity and soluble collagen content in all of the groups were roughly similar. These results suggest that increased dermal oxygen tension attenuates angiogenesis and wrinkle formation following acute UVB irradiation.
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PMID:Increased oxygen tension attenuates acute ultraviolet-B-induced skin angiogenesis and wrinkle formation. 2050 8