Acid Phosphatase Activity in Human Blood Cells

Goldberg, Avishay; Barka, Tibor

doi:10.1038/195297a0

Cited by 221 publications

(56 citation statements)

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“…Cells were then fixed (inhibitor only) or treated with CT for 20 min before fixing (CT only, inhibitor plus CT). The fixed cells were stained with toluidine blue or TRAP-stained (50,51), and the area of at least 70 osteoclasts/ group was measured with a computerized system for histomorphometry (Osteometrics, Atlanta, GA).…”

Section: Methodsmentioning

confidence: 99%

Calpain Is Required for Normal Osteoclast Function and Is Down-regulated by Calcitonin

Marzia

Chiusaroli

Neff

et al. 2006

Journal of Biological Chemistry

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Osteoclast motility is thought to depend on rapid podosome assembly and disassembly. Both -calpain and m-calpain, which promote the formation and disassembly of focal adhesions, were observed in the podosome belt of osteoclasts. Calpain inhibitors disrupted the podosome belt, blocked the constitutive cleavage of the calpain substrates filamin A, talin, and Pyk2, which are enriched in the podosome belt, induced osteoclast retraction, and reduced osteoclast motility and bone resorption. The motility and resorbing activity of -calpain ؊/؊ osteoclast-like cells were also reduced, indicating that -calpain is required for normal osteoclast activity. Histomorphometric analysis of tibias from -calpain ؊/؊ mice revealed increased osteoclast numbers and decreased trabecular bone volume that was apparent at 10 weeks but not at 5 weeks of age. In vitro studies suggested that the increased osteoclast number in the -calpain ؊/؊ bones resulted from increased osteoclast survival, not increased osteoclast formation. Calcitonin disrupted the podosome ring, induced osteoclast retraction, and reduced osteoclast motility and bone resorption in a manner similar to the effects of calpain inhibitors and had no further effect on these parameters when added to osteoclasts pretreated with calpain inhibitors. Calcitonin inhibited the constitutive cleavage of a fluorogenic calpain substrate and transiently blocked the constitutive cleavage of filamin A, talin, and Pyk2 by a protein kinase C-dependent mechanism, demonstrating that calcitonin induces the inhibition of calpain in osteoclasts. These results indicate that calpain activity is required for normal osteoclast activity and suggest that calcitonin inhibits osteoclast bone resorbing activity in part by down-regulating calpain activity.Osteoclasts are large multinucleated cells of the monocyte-macrophage lineage that play a critical role in skeletal development and repair and in calcium homeostasis by resorbing mineralized cartilage and bone. They display a high degree of motility, which is required for normal bone resorbing activity. As in other highly motile cells, the integrinbased attachment complexes of osteoclasts are podosomes, which are structurally and functionally distinct from focal adhesions (1-6). Although many of the same proteins are present in both podosomes and focal adhesions, podosomes are notably more dynamic, undergoing assembly and disassembly within minutes (5-7). The rapid and cyclic podosome assembly and disassembly and their dynamic interaction with elements of the actin cytoskeleton are thought to be critical for the high motility of osteoclasts (7).Recently, calpains have been found to play crucial roles in the regulation of motility in cells such as fibroblasts that form focal adhesions (8). Calpains are a family of cytosolic cysteine proteases, many of which are Ca 2ϩ -dependent, that catalyze the limited cleavage of specific proteins during regulatory signaling (9, 10). The most studied members of the calpain family are the ubiquitously expressed -calpain ...

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Section: Methodsmentioning

confidence: 99%

Calpain Is Required for Normal Osteoclast Function and Is Down-regulated by Calcitonin

Marzia

Chiusaroli

Neff

et al. 2006

Journal of Biological Chemistry

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“…Для суждения об активности аминооксидазного пути окисления моноаминов определяли моноамин-оксидазу (МАО) [10], для оценки катаболического пути обмена в лимфоцитах -фермент лизосомнеспе-цифическую кислую фосфатазу (КФ) [11]. Активность дегидрогеназ и МАО выражали количеством гранул формазана в 1 клетке -гр/кл, а активность КФ -ин-дексом Kaplow [12].…”

Section: характеристика детей и методы исследованияunclassified

Specific features of the lymphocyte enzyme status in newborn infants with the hypotrophic type of intrauterine growth retardation

Новицкая¹,

Грицинская²

2016

Ross. vestn. perinatol. pediatr.

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Нарушение внутриутробного роста и развития плода остается одной из актуальных проблем акушерства и перинатологии. Значимость задержки внутриутробного развития определяется ее большим удельным весом в структуре перинатальной смерт-ности и заболеваемости новорожденных, а также не-благоприятным медико-биологическим и социаль-ным прогнозом в будущем [1][2][3][4][5].Термин «задержка внутриутробного развития» используют для обозначения хронического рас-стройства питания плода, сопровождающегося от-ставанием его внутриутробного развития, физиче-ских параметров, клинической и функциональной незрелостью ряда органов и систем, снижением им-мунологической реактивности и метаболическими расстройствами. Принято выделять три клинических варианта задержки внутриутробного развития [2]: гипотрофический, гипопластический и диспласти-ческий. В англоязычной литературе вместо термина «гипотрофический вариант» используют понятие «асимметричная задержка внутриутробного разви-тия», а гипопластический и диспластический вари-анты объединяют понятием «симметричная задержка внутриутробного развития».Гипотрофический вариант характеризуется практически нормальным ростом скелета и голо-вы, но снижением в различной степени количества подкожного жира и мышечной массы. Полагают, что подобный вариант формируется на более позд-них сроках беременности. Дети с данным вариан-том задержки внутриутробного развития имеют высокий риск ранних осложнений в неонаталь- © Коллектив авторов, 2016Ros Vestn Perinatol Pediat 2016; 3:46-50 DOI: 10.21508/1027 3:46-50 DOI: 10.21508/ -4065-2016 Адрес для корреспонденции: Новицкая Валентина Петровна -д.б.н., ст. н. сотр. лаборатории клинической патофизиологии НИИ медицин-ских проблем севера Грицинская Вера Людвиговна -д.м.н., гл. н. сотр. той же лаборатории 660022 Красноярск, ул. Партизана Железняка, д. Results. It was ascertained that the activity of SDH, GPDH, and LDH was higher on 5 day of life and that of NADFH2-diaphorase was lower in infants with intrauterine growth retardation than in apparently healthy neonates. Desynchronosis of the metabolic pathways was established in the dynamics of early ontogenesis. Conclusion. It is necessary to rationally correct standard treatment regimens, by taking into account the found metabolic features in infants with intrauterine growth retardation under the conditions of Yakutia.

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“…Активность тартратрезистентной кислой фосфа тазы в лимфоцитах на биочипе определялась методом Гольдберга-Барки [6] с добавлением тартрата натрия в концентрации 7,5 мг/мл.…”

Section: ф у н д а м е н т а л ь н ы е и с с л е д о в а н и я в п р unclassified

Cell-binding microarray application in diagnosis of hairy cell leukemia

Khvastunova¹,

Al-Radi²,

Kapranov³

et al. 2015

Onkogematologiâ

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Acid Phosphatase Activity in Human Blood Cells

Cited by 221 publications

References 1 publication

Calpain Is Required for Normal Osteoclast Function and Is Down-regulated by Calcitonin

Calpain Is Required for Normal Osteoclast Function and Is Down-regulated by Calcitonin

Specific features of the lymphocyte enzyme status in newborn infants with the hypotrophic type of intrauterine growth retardation

Cell-binding microarray application in diagnosis of hairy cell leukemia

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