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Cellular Hypertrophy (cellular + hypertrophy)
Selected AbstractsThe Assembly and Remodeling of the Extracellular Matrix in the Growth Plate in Relationship to Mineral Deposition and Cellular Hypertrophy: An In Situ Study of Collagens II and IX and Proteoglycan,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 2 2002Fackson Mwale Abstract The recent development of new specific immunoassays has provided an opportunity to study the assembly and resorption of type II and IX collagens of the extracellular matrix in relationship to endochondral calcification in situ. Here, we describe how in the bovine fetal physis prehypertrophic chondrocytes deposit an extensive extracellular matrix that, initially, is rich in both type II and type IX collagens and proteoglycan (PG; principally, aggrecan). The majority of the ,1(IX)-chains lack the NC4 domain consistent with our previous studies with cultured chondrocytes. During assembly, the molar ratio of type II/COL2 domain of the ,1(IX)-chain varied from 8:1 to 25:1. An increase in the content of Ca2+ and inorganic phosphate (Pi) was initiated in the prehypertrophic zone when the NC4 domain was removed selectively from the ,1(IX)-chain. This was followed by the progressive loss of the ,1(IX) COL2 domain and type II collagen. In the hypertrophic zone, the Ca2+/Pi molar ratio ranged from 1.56 to a maximum of 1.74, closely corresponding to that of mature hydroxyapatite (1.67). The prehypertrophic zone had an average ratio Ca2+/Pi ranging from 0.25 to 1, suggesting a phase transformation. At hypertrophy, when mineral content was maximal, type II collagen was reduced maximally in content coincident with a peak of cleavage of this molecule by collagenase when matrix metalloproteinase 13 (MMP-13) expression was maximal. In contrast, PG (principally aggrecan) was retained when hydroxyapatite was formed consistent with the view that this PG does not inhibit and might promote calcification in vivo. Taken together with earlier studies, these findings show that matrix remodeling after assembly is linked closely to initial changes in Ca2+ and Pi to subsequent cellular hypertrophy and mineralization. These changes involve a progressive and selective removal of types II and IX collagens with the retention of the PG aggrecan. [source] Age-Related Increase in Atrial Fibrillation Induced by Transvenous Catheter-Based Atrial Burst Pacing: An In Vivo Rat Model of Inducible Atrial FibrillationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2010DONGZHU XU M.D. AF Rat Model Induced by Transvenous Catheter Pacing.,Introduction: Large animal models of atrial fibrillation (AF) are well established, but limited experimental reports exist on small animal models. We sought to develop an in vivo rat model of AF using a transvenous catheter and to evaluate the model's underlying characteristics. Methods and Results: Echocardiogram, surface electrocardiogram (ECG), and atrial effective refractory period (AERP) were recorded at baseline in young (3 months) and middle-aged (9 months) Wistar rats. AF inducibility and duration were measured through transvenous electrode catheter in young (n = 11) and middle-aged rats (n = 11) and middle-aged rats treated with either pilsicainide (1 mg/kg iv, n = 7) or amiodarone (10 mg/kg iv, n = 9). Degrees of interstitial fibrosis and cellular hypertrophy in the atria were assessed histologically. The P-wave duration and AERP were significantly longer and echocardiographic left atrial dimension significantly larger in middle-aged versus young rats. AF was inducible in >90% of all procedures in both untreated rat groups, whereas AF inducibility was reduced by the antiarrhythmic drugs. The AF duration was significantly longer in middle-aged than in young rats and was significantly shortened by treatment with either pilsicainide or amiodarone. Histologic analysis revealed significant increases in atrial interstitial fibrosis and cellular diameter in middle-aged versus young rats. Conclusions: Transvenous catheter-based AF is significantly longer in middle-aged than in young rats and is markedly reduced by treatment with antiarrhythmic drugs. This rat model of AF is simple, reproducible, and reliable for examining pharmacologic effects on AF and studying the process of atrial remodeling.(J Cardiovasc Electrophysiol, Vol. 21, pp. 88,93, January 2010) [source] Adrenergic regulation of cardiac myocyte apoptosisJOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2001Krishna Singh The direct effects of catecholamines on cardiac myocytes may contribute to both normal physiologic adaptation and pathologic remodeling, and may be associated with cellular hypertrophy, apoptosis, and alterations in contractile function. Norepinephrine (NE) signals via ,- and ,-adrenergic receptors (AR) that are coupled to G-proteins. Pharmacologic studies of cardiac myocytes in vitro demonstrate that stimulation of ,1 -AR induces apoptosis which is cAMP-dependent and involves the voltage-dependent calcium influx channel. In contrast, stimulation of ,2 -AR exerts an anti-apoptotic effect which appears to be mediated by a pertussis toxin-sensitive G protein. Stimulation of ,1 -AR causes myocyte hypertrophy and may exert an anti-apoptotic action. In transgenic mice, myocardial overexpression of either ,1 -AR or G,s is associated with myocyte apoptosis and the development of dilated cardiomyopathy. Myocardial overexpression of ,2 -AR at low levels results in improved cardiac function, whereas expression at high levels leads to dilated cardiomyopathy. Overexpression of wildtype ,1B -AR does not result in apoptosis, whereas overexpression of G,q results in myocyte hypertrophy and/or apoptosis depending on the level of expression. Differential activation of the members of the mitogen-activated protein kinase (MAPK) superfamily and production of reactive oxygen species appear to play a key role in mediating the actions of adrenergic pathways on myocyte apoptosis and hypertrophy. This review summarizes current knowledge about the molecular and cellular mechanisms involved in the regulation of cardiac myocyte apoptosis via stimulation of adrenergic receptors and their coupled effector pathways. © 2001 Wiley-Liss, Inc. [source] Glial Limitans Elasticity Subjacent to the Supraoptic NucleusJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2004A. K. Salm Abstract Two previous studies from our laboratory have indicated that the ventral glial limitans subjacent to the hypothalamic supraoptic nucleus (SON-VGL) undergoes a reversible thinning upon chronic activation of the magnocellular neuroendocrine cells (MNCs) of the supraoptic nucleus (SON). Numerous other studies have shown that MNC somata hypertrophy with activation. One aim of the current study was to understand better how SON-VGL thinning occurs. A second aim was to quantify overall changes of the MNC somata region due to cellular hypertrophy to compare relative changes in dimensions. Here, we undertook a light microscopic stereological investigation of the SON and the subjacent SON-VGL of Nissl stained material under basal and activated conditions. Astrocyte numbers in the underlying SON-VGL remained stable across hydration state as did the overall volume of the SON-VGL and dendritic zone reference area. How these data are consistent with our earlier observations of SON-VGL thinning was resolved by the finding of a highly significant, 30% increase in the mediolateral dimension of the SON-VGL in dehydrated rats. These observations fit well with previous work from our laboratory that demonstrates a reorientation of SON-VGL astrocytes, from vertical to horizontal, which occurs in the activated SON-VGL. We found a significant, approximately 54%, increase in the overall volume of the MNC region of the SON. No significant rostrocaudal lengthening of the SON was detected, although a trend was evident. All the observed changes reversed with rehydration. These data indicate that elasticity of the SON-VGL acts to accommodate the volume expansion of the MNCs and enables the SON-VGL to continue as an interface between the underlying cerebrospinal fluid in the subarachnoid space and the expanded SON above. [source] | ||||||||||