| β-Thromboglobulin | |||||||
|---|---|---|---|---|---|---|---|
| Identifiers | |||||||
| Symbol | CXCL7 | ||||||
| Alt. symbols | CTAP3, CXCL7, SCYB7, TGB1, THBGB1 | ||||||
| NCBI gene | 5473 | ||||||
| HGNC | 9240 | ||||||
| OMIM | 121010 | ||||||
| RefSeq | NP_002695 | ||||||
| UniProt | P02775 | ||||||
| Other data | |||||||
| Locus | Chr. 4 q13.3 | ||||||
| |||||||
β-Thromboglobulin (β-TG), or beta-thromboglobulin, is a chemokine protein secreted by platelets. [1] [2] It is a type of chemokine (C-X-C motif) ligand 7. [3] Along with platelet factor 4 (PF4), β-TG is one of the best-characterized platelet-specific proteins. [4] β-TG and PF4 are stored in platelet alpha granules and are released during platelet activation. [1] [4] [5] As a result, they are useful markers of platelet activation. [1] [4] β-TG also has multiple biological activities, for instance being involved in maturation of megakaryocytes. [6]
Biological actions
β-TG is a chemoattractant, strongly for fibroblasts and weakly for neutrophils. It is a stimulator of mitogenesis, extracellular matrix synthesis, glucose metabolism, and plasminogen activator synthesis in human fibroblasts. [5]
β-TG also affects megakaryocyte maturation, and thus helps in regulating platelet production. [5]
Clinical uses
Levels of β-TG is used to index platelet activation. It is measured by ELISA in blood plasma or urine, and often in conjunction with PF4. [5]
Influences
β-TG levels may increase with age. [7] It is elevated in diabetes mellitus. [8]
β-TG levels have been found to be increased by treatment with the synthetic estrogen ethinylestradiol, though were not significantly increased by the natural estrogen estradiol valerate. [9] [10] [11] [12] Levels of β-TG have also been found to be increased or unchanged during normal pregnancy. [13]
References
- ^ a b c Sharma G, Berger JS (August 2011). "Platelet activity and cardiovascular risk in apparently healthy individuals: a review of the data". J Thromb Thrombolysis. 32 (2): 201–8. doi: 10.1007/s11239-011-0590-9. PMID 21562837. S2CID 23686294.
- ^ Kaplan KL, Owen J (February 1981). "Plasma levels of beta-thromboglobulin and platelet factor 4 as indices of platelet activation in vivo". Blood. 57 (2): 199–202. doi: 10.1182/blood.V57.2.199.199. PMID 6160890.
- ^ Pillai MM, Iwata M, Awaya N, Graf L, Torok-Storb B (May 2006). "Monocyte-derived CXCL7 peptides in the marrow microenvironment". Blood. 107 (9): 3520–6. doi: 10.1182/blood-2005-10-4285. PMC 1895768. PMID 16391012.
- ^ a b c Cella G, Scattolo N, Girolami A, Sasahara AA (1984). "Are platelet factor 4 and beta-thromboglobulin markers of cardiovascular disorders?". Ric Clin Lab. 14 (1): 9–18. doi: 10.1007/BF02905035. PMID 6203164. S2CID 58519828.
- ^ a b c d Cytokines & Cells Online Pathfinder Encyclopaedia → Beta-Thromboglobulin Retrieved on August 17, 2009
- ^ Chung-Eun Ha; N. V. Bhagavan (24 April 2015). Essentials of Medical Biochemistry: With Clinical Cases (2 ed.). Academic Press. pp. 652–. ISBN 978-0-12-416697-4. OCLC 1006915388.
- ^ Martinelli I, Bucciarelli P, Mannucci PM (February 2010). "Thrombotic risk factors: basic pathophysiology". Crit Care Med. 38 (2 Suppl): S3–9. doi: 10.1097/CCM.0b013e3181c9cbd9. PMID 20083911. S2CID 34486553.
- ^ Page 121 in: Sterne, Jonathan; Kirkwood, Betty R. (2003). Essential medical statistics. Oxford: Blackwell Science. ISBN 0-86542-871-9.
- ^ Farris M, Bastianelli C, Rosato E, Brosens I, Benagiano G (October 2017). "Pharmacodynamics of combined estrogen-progestin oral contraceptives: 2. effects on hemostasis". Expert Rev Clin Pharmacol. 10 (10): 1129–1144. doi: 10.1080/17512433.2017.1356718. PMID 28712325. S2CID 205931204.
- ^ Kluft C, Lansink M (July 1997). "Effect of oral contraceptives on haemostasis variables". Thromb Haemost. 78 (1): 315–26. doi: 10.1055/s-0038-1657546. PMID 9198173.
- ^ Kuhl, H (1998). "Adverse effects of estrogen treatment: natural vs. synthetic estrogens". In Lippert, T. H.; Mueck, A. O.; Ginsburg, J. (eds.). Sex Steroids and the Cardiovascular System: The Proceedings of the 1st Interdisciplinary Workshop, Tuebingen, Germany, October 1996. London/New York: Parthenon. pp. 201–210. ISBN 9781850709565.
- ^ Lindberg UB, Crona N, Stigendal L, Teger-Nilsson AC, Silfverstolpe G (February 1989). "A comparison between effects of estradiol valerate and low dose ethinyl estradiol on haemostasis parameters". Thromb Haemost. 61 (1): 65–9. doi: 10.1055/s-0038-1646528. PMID 2526387.
- ^ Hellgren M (April 2003). "Hemostasis during normal pregnancy and puerperium". Semin Thromb Hemost. 29 (2): 125–30. doi: 10.1055/s-2003-38897. PMID 12709915.
.svg){kind=small} | This biochemistry article is a stub. You can help Wikipedia by expanding it. |
 | This hematology article is a stub. You can help Wikipedia by expanding it. |
| β-Thromboglobulin | |||||||
|---|---|---|---|---|---|---|---|
| Identifiers | |||||||
| Symbol | CXCL7 | ||||||
| Alt. symbols | CTAP3, CXCL7, SCYB7, TGB1, THBGB1 | ||||||
| NCBI gene | 5473 | ||||||
| HGNC | 9240 | ||||||
| OMIM | 121010 | ||||||
| RefSeq | NP_002695 | ||||||
| UniProt | P02775 | ||||||
| Other data | |||||||
| Locus | Chr. 4 q13.3 | ||||||
| |||||||
β-Thromboglobulin (β-TG), or beta-thromboglobulin, is a chemokine protein secreted by platelets. [1] [2] It is a type of chemokine (C-X-C motif) ligand 7. [3] Along with platelet factor 4 (PF4), β-TG is one of the best-characterized platelet-specific proteins. [4] β-TG and PF4 are stored in platelet alpha granules and are released during platelet activation. [1] [4] [5] As a result, they are useful markers of platelet activation. [1] [4] β-TG also has multiple biological activities, for instance being involved in maturation of megakaryocytes. [6]
Biological actions
β-TG is a chemoattractant, strongly for fibroblasts and weakly for neutrophils. It is a stimulator of mitogenesis, extracellular matrix synthesis, glucose metabolism, and plasminogen activator synthesis in human fibroblasts. [5]
β-TG also affects megakaryocyte maturation, and thus helps in regulating platelet production. [5]
Clinical uses
Levels of β-TG is used to index platelet activation. It is measured by ELISA in blood plasma or urine, and often in conjunction with PF4. [5]
Influences
β-TG levels may increase with age. [7] It is elevated in diabetes mellitus. [8]
β-TG levels have been found to be increased by treatment with the synthetic estrogen ethinylestradiol, though were not significantly increased by the natural estrogen estradiol valerate. [9] [10] [11] [12] Levels of β-TG have also been found to be increased or unchanged during normal pregnancy. [13]
References
- ^ a b c Sharma G, Berger JS (August 2011). "Platelet activity and cardiovascular risk in apparently healthy individuals: a review of the data". J Thromb Thrombolysis. 32 (2): 201–8. doi: 10.1007/s11239-011-0590-9. PMID 21562837. S2CID 23686294.
- ^ Kaplan KL, Owen J (February 1981). "Plasma levels of beta-thromboglobulin and platelet factor 4 as indices of platelet activation in vivo". Blood. 57 (2): 199–202. doi: 10.1182/blood.V57.2.199.199. PMID 6160890.
- ^ Pillai MM, Iwata M, Awaya N, Graf L, Torok-Storb B (May 2006). "Monocyte-derived CXCL7 peptides in the marrow microenvironment". Blood. 107 (9): 3520–6. doi: 10.1182/blood-2005-10-4285. PMC 1895768. PMID 16391012.
- ^ a b c Cella G, Scattolo N, Girolami A, Sasahara AA (1984). "Are platelet factor 4 and beta-thromboglobulin markers of cardiovascular disorders?". Ric Clin Lab. 14 (1): 9–18. doi: 10.1007/BF02905035. PMID 6203164. S2CID 58519828.
- ^ a b c d Cytokines & Cells Online Pathfinder Encyclopaedia → Beta-Thromboglobulin Retrieved on August 17, 2009
- ^ Chung-Eun Ha; N. V. Bhagavan (24 April 2015). Essentials of Medical Biochemistry: With Clinical Cases (2 ed.). Academic Press. pp. 652–. ISBN 978-0-12-416697-4. OCLC 1006915388.
- ^ Martinelli I, Bucciarelli P, Mannucci PM (February 2010). "Thrombotic risk factors: basic pathophysiology". Crit Care Med. 38 (2 Suppl): S3–9. doi: 10.1097/CCM.0b013e3181c9cbd9. PMID 20083911. S2CID 34486553.
- ^ Page 121 in: Sterne, Jonathan; Kirkwood, Betty R. (2003). Essential medical statistics. Oxford: Blackwell Science. ISBN 0-86542-871-9.
- ^ Farris M, Bastianelli C, Rosato E, Brosens I, Benagiano G (October 2017). "Pharmacodynamics of combined estrogen-progestin oral contraceptives: 2. effects on hemostasis". Expert Rev Clin Pharmacol. 10 (10): 1129–1144. doi: 10.1080/17512433.2017.1356718. PMID 28712325. S2CID 205931204.
- ^ Kluft C, Lansink M (July 1997). "Effect of oral contraceptives on haemostasis variables". Thromb Haemost. 78 (1): 315–26. doi: 10.1055/s-0038-1657546. PMID 9198173.
- ^ Kuhl, H (1998). "Adverse effects of estrogen treatment: natural vs. synthetic estrogens". In Lippert, T. H.; Mueck, A. O.; Ginsburg, J. (eds.). Sex Steroids and the Cardiovascular System: The Proceedings of the 1st Interdisciplinary Workshop, Tuebingen, Germany, October 1996. London/New York: Parthenon. pp. 201–210. ISBN 9781850709565.
- ^ Lindberg UB, Crona N, Stigendal L, Teger-Nilsson AC, Silfverstolpe G (February 1989). "A comparison between effects of estradiol valerate and low dose ethinyl estradiol on haemostasis parameters". Thromb Haemost. 61 (1): 65–9. doi: 10.1055/s-0038-1646528. PMID 2526387.
- ^ Hellgren M (April 2003). "Hemostasis during normal pregnancy and puerperium". Semin Thromb Hemost. 29 (2): 125–30. doi: 10.1055/s-2003-38897. PMID 12709915.
|
| This biochemistry article is a stub. You can help Wikipedia by expanding it. |
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| This hematology article is a stub. You can help Wikipedia by expanding it. |