On the in Vitro Behaviour of Mouse Submaxillary Gland Cells

1973 ◽  
Vol 13 (2) ◽  
pp. 441-445
Author(s):  
MARIA LUISA MARCANTE
Keyword(s):  
Endoplasmic Reticulum ◽  
Lactate Dehydrogenase ◽  
Submaxillary Gland ◽  
Biochemical Properties ◽  
Dark Cells ◽  
Submaxillary Glands ◽  
Mouse Submaxillary Gland ◽  
Good Agreement

Investigations on the morphological features and some biochemical properties of cells isolated from mouse C3H/He (IRE/Ar) submaxillary glands cultivated in vitro are reported. Two types of cells have been recognized: the dark cells differ from the light in the shape of their mitochondria, and number of vacuoles, while endoplasmic reticulum is absent. The enzymic activities, which have been tested, are phosphofructokinase, pyruvate kinase, amylase and lactate dehydrogenase. The values for enzyme activities in vitro are in good agreement with those obtained for submaxillary gland in vivo. Therefore, it can be concluded that during their growth in vitro cells from submaxillary glands retain their enzymic properties.

Analysis of elongating morphogenesis of quail anterior submaxillary gland: absence of localized cell proliferation

Development ◽  
1981 ◽  
Vol 62 (1) ◽  
pp. 229-239
Author(s):  
Hiroyuki Nogawa
Keyword(s):  
Cell Proliferation ◽  
Basement Membrane ◽  
Regional Differences ◽  
Submaxillary Gland ◽  
Mesenchymal Cells ◽  
Submaxillary Glands ◽  
Parallel Direction ◽  
Recombination Experiments

Quail anterior submaxillary glands elongated extensively without branching (more than sevenfold) from 8 to 10 incubation days. Investigation of mitotic activity of the rudiments in vivo showed no localized cell proliferation throughout the rudiments, and recombination experiments in vitro to examine regional differences in mitogenic activity of the surrounding mesenchyme also showed that no mesenchymal region specifically stimulates the epithelial cell proliferation. Histological observation of the rudiments showed that epithelial cells did not lengthen in a parallel direction to the long axis of the rudiment, and that mesenchymal cells encircled the epithelial cord perpendicularly to its axis. The basement membrane was obscure in the distal end of the rudiments, while it was easily detected in the other part of the rudiments. These results suggest that the elongating morphogenesis of the anterior submaxillary rudiments is not achieved by localized cell proliferation but by almost uniformly distributed cell proliferation, and mesenchymal cells surrounding the rudiment or the basement membrane may be involved in the controlling mechanisms of the elongating morphogenesis.

scholarly journals NADP+-Preferring d-Lactate Dehydrogenase from Sporolactobacillus inulinus

2015 ◽  
Vol 81 (18) ◽  
pp. 6294-6301 ◽  
Author(s):  
Lingfeng Zhu ◽  
Xiaoling Xu ◽  
Limin Wang ◽  
Hui Dong ◽  
Bo Yu ◽  
...  
Keyword(s):  
Lactate Dehydrogenase ◽  
Catalytic Mechanism ◽  
High Specificity ◽  
Biochemical Properties ◽  
Enzymatic System ◽  
Content Type ◽  
Wide Range ◽  
Lactate Dehydrogenases

ABSTRACTHydroxy acid dehydrogenases, includingl- andd-lactate dehydrogenases (L-LDH and D-LDH), are responsible for the stereospecific conversion of 2-keto acids to 2-hydroxyacids and extensively used in a wide range of biotechnological applications. A common feature of LDHs is their high specificity for NAD+as a cofactor. An LDH that could effectively use NADPH as a coenzyme could be an alternative enzymatic system for regeneration of the oxidized, phosphorylated cofactor. In this study, ad-lactate dehydrogenase from aSporolactobacillus inulinusstrain was found to use both NADH and NADPH with high efficiencies and with a preference for NADPH as its coenzyme, which is different from the coenzyme utilization of all previously reported LDHs. The biochemical properties of the D-LDH enzyme were determined by X-ray crystal structural characterization andin vivoandin vitroenzymatic activity analyses. The residue Asn174was demonstrated to be critical for NADPH utilization. Characterization of the biochemical properties of this enzyme will contribute to understanding of the catalytic mechanism and provide referential information for shifting the coenzyme utilization specificity of 2-hydroxyacid dehydrogenases.

Sympathetic nervous system and renin release from submaxillary glands in vitro

1976 ◽  
Vol 231 (2) ◽  
pp. 551-554 ◽  
Author(s):  
AM Michelakis ◽  
JW Menzie ◽  
H Yoshida
Keyword(s):  
Direct Action ◽  
Submaxillary Gland ◽  
Renin Release ◽  
Adrenergic Agonists ◽  
Beta Adrenergic ◽  
Submaxillary Glands ◽  
Beta Adrenergic Agonists ◽  
Camp Levels

We previously reported that alpha- but not beta-adrenergic agonists stimulate renin release from mouse submaxillary glands in vivo. The present studies were undertaken to determine if these in vivo effects were due to a direct action on the submaxillary glands and to find out if cyclic AMP (cAMP) might be involved in submaxillary renin release. Pooled mouse submaxillary gland slices were incubated in Krebs-Ringer bicarbonate medium following a preincubation period, and renin release was measured by a radioimmunoassay for the direct measurement of submaxillary gland renin. Tissue cAMP levels were also measured. Addition of the alpha-adrenergic agonists, phenylephrine or norepinephrine, significantly increased renin release (P less than 0.01 vs. control) while decreasing tissue cAMP levels (P less than 0.01 vs. control). In contrast, addition of the beta-adrenergic agonist isoproterenol markedly increased cAMP levels (P less than 0.01 vs. control) and decreased renin release (P less than 0.05 vs. control). Pretreatment of the slices with the alpha-blocker phenoxy genzamine inhibited the effect of phenylephrine. These results indicate that alpha-adrenergic agonists cause renin release from submaxillary glands which is accompanied by a fall in tissue cAMP levels. This is in contrast to renin release from the kidney which is stimulated by beta-adrenergic agonists.

scholarly journals Dehydrodiisoeugenol inhibits colorectal cancer growth by endoplasmic reticulum stress-induced autophagic pathways

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Changhong Li ◽  
Kui Zhang ◽  
Guangzhao Pan ◽  
Haoyan Ji ◽  
Chongyang Li ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Growth ◽  
Er Stress ◽  
Cancer Cells ◽  
Tumor Xenograft ◽  
Anticancer Activities ◽  
Colorectal Cancer Cells

Abstract Background Dehydrodiisoeugenol (DEH), a novel lignan component extracted from nutmeg, which is the seed of Myristica fragrans Houtt, displays noticeable anti-inflammatory and anti-allergic effects in digestive system diseases. However, the mechanism of its anticancer activity in gastrointestinal cancer remains to be investigated. Methods In this study, the anticancer effect of DEH on human colorectal cancer and its underlying mechanism were evaluated. Assays including MTT, EdU, Plate clone formation, Soft agar, Flow cytometry, Electron microscopy, Immunofluorescence and Western blotting were used in vitro. The CDX and PDX tumor xenograft models were used in vivo. Results Our findings indicated that treatment with DEH arrested the cell cycle of colorectal cancer cells at the G1/S phase, leading to significant inhibition in cell growth. Moreover, DEH induced strong cellular autophagy, which could be inhibited through autophagic inhibitors, with a rction in the DEH-induced inhibition of cell growth in colorectal cancer cells. Further analysis indicated that DEH also induced endoplasmic reticulum (ER) stress and subsequently stimulated autophagy through the activation of PERK/eIF2α and IRE1α/XBP-1 s/CHOP pathways. Knockdown of PERK or IRE1α significantly decreased DEH-induced autophagy and retrieved cell viability in cells treated with DEH. Furthermore, DEH also exhibited significant anticancer activities in the CDX- and PDX-models. Conclusions Collectively, our studies strongly suggest that DEH might be a potential anticancer agent against colorectal cancer by activating ER stress-induced inhibition of autophagy.

Dietary (-)-epicatechin mitigates high fat-induced apoptosis, oxidative and endoplasmic reticulum stress in pancreatic β-cells both in vivo and in vitro

2021 ◽  
Vol 165 ◽  
pp. 44
Author(s):  
Eleonora Cremonini ◽  
Maëlys Rouget ◽  
Solenne Arredi ◽  
Charlotte Devulder-Mercier ◽  
Robin Cellier ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
High Fat ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Induced Apoptosis

Mesenchymal control over elongating and branching morphogenesis in salivary gland development

Development ◽  
1981 ◽  
Vol 66 (1) ◽  
pp. 209-221
Author(s):  
Hiroyuki Nogawa ◽  
Takeo Mizuno
Keyword(s):  
Salivary Gland ◽  
Salivary Glands ◽  
Submaxillary Gland ◽  
Branching Morphogenesis ◽  
Mouse Submaxillary Gland ◽  
Gland Development

Recombination of the epithelium and mesenchyme between quail anterior submaxillary gland (elongating type) and quail anterior lingual or mouse submaxillary gland (branching type) was effected in vitro to clarify whether the elongating morphogenesis was directed by the epithelial or the mesenchymal component. Quail anterior submaxillary epithelium recombined with quail anterior lingual or mouse submaxillary mesenchyme came to branch. Conversely, quail anterior lingual or 12-day mouse submaxillary epithelium recombined with quail anterior submaxillary mesenchyme came to elongate, though the mesenchyme was less effective with 13-day mouse submaxillary epithelium. These results suggest that the elongating or branching morphogenesis of quail salivary glands is controlled by the mesenchyme.

Influence of pilocarpine on transport by salivary gland slices

1963 ◽  
Vol 205 (5) ◽  
pp. 1058-1062 ◽  
Author(s):  
L. H. Schneyer ◽  
C. A. Schneyer
Keyword(s):  
Salivary Gland ◽  
Submaxillary Gland ◽  
Nitrogen Atmosphere ◽  
Total Water ◽  
Early Effect ◽  
Apparent Loss ◽  
Inulin Space ◽  
Total Tissue

Effects of pilocarpine on net movements of water and electrolytes in gland cells were investigated in vitro, using slices from submaxillary gland of rat. Slices were depleted of K, and loaded with Na, Cl, and water, by incubation in Krebs-Ringer phosphate with nitrogen atmosphere. After this, the slices were transferred to Krebs-Ringer phosphate with oxygen atmosphere. During this period with O2, pilocarpine caused apparent loss of water from cells, since tissue total water decreased and inulin space remained almost unchanged. Without pilocarpine during this time, water in cells increased. Electrolyte movements were also affected by pilocarpine. Specifically, there occurred reduction in net accumulation of K in total tissue and cells. Reduction in net extrusion of Na was suggested. Since, in vivo, an early effect of stimulation involves depletion of gland K, it appears that the current observations have relevance to normal secretion to the extent, at least, that in both circumstances stimulating agents reduce the ability of the cells to maintain stores of K.

scholarly journals A cellular endolysosome-modulating pore-forming protein from a toad is negatively regulated by its paralog under oxidizing conditions

2020 ◽  
Vol 295 (30) ◽  
pp. 10293-10306 ◽  
Author(s):  
Qiquan Wang ◽  
Xianling Bian ◽  
Lin Zeng ◽  
Fei Pan ◽  
Lingzhen Liu ◽  
...  
Keyword(s):  
Disulfide Bond ◽  
Cell Biology ◽  
Biochemical Properties ◽  
Bacterial Toxin ◽  
Cell Physiology ◽  
Dependent Manner ◽  
Membrane Pore ◽  
Intracellular Vesicles

Endolysosomes are key players in cell physiology, including molecular exchange, immunity, and environmental adaptation. They are the molecular targets of some pore-forming aerolysin-like proteins (ALPs) that are widely distributed in animals and plants and are functionally related to bacterial toxin aerolysins. βγ-CAT is a complex of an ALP (BmALP1) and a trefoil factor (BmTFF3) in the firebelly toad (Bombina maxima). It is the first example of a secreted endogenous pore-forming protein that modulates the biochemical properties of endolysosomes by inducing pore formation in these intracellular vesicles. Here, using a large array of biochemical and cell biology methods, we report the identification of BmALP3, a paralog of BmALP1 that lacks membrane pore-forming capacity. We noted that both BmALP3 and BmALP1 contain a conserved cysteine in their C-terminal regions. BmALP3 was readily oxidized to a disulfide bond-linked homodimer, and this homodimer then oxidized BmALP1 via disulfide bond exchange, resulting in the dissociation of βγ-CAT subunits and the elimination of biological activity. Consistent with its behavior in vitro, BmALP3 sensed environmental oxygen tension in vivo, leading to modulation of βγ-CAT activity. Interestingly, we found that this C-terminal cysteine site is well conserved in numerous vertebrate ALPs. These findings uncover the existence of a regulatory ALP (BmALP3) that modulates the activity of an active ALP (BmALP1) in a redox-dependent manner, a property that differs from those of bacterial toxin aerolysins.

Effects of (+)-Catechin in vitro and in vivo on Disturbances Produced in Rat Liver Endoplasmic Reticulum by Carbon Tetrachloride

1977 ◽  
Vol 5 (4) ◽  
pp. 1029-1032 ◽  
Author(s):  
OLIVIERO DANNI ◽  
BARBARA C. SAWYER ◽  
TREVOR F. SLATER
Keyword(s):  
Endoplasmic Reticulum ◽  
Carbon Tetrachloride ◽  
Rat Liver

scholarly journals Overexpression of SERCA2a Alleviates Cardiac Microvascular Ischemic Injury by Suppressing Mfn2-Mediated ER/Mitochondrial Calcium Tethering

2021 ◽  
Vol 9 ◽  
Author(s):  
Feng Tian ◽  
Ying Zhang
Keyword(s):  
Endoplasmic Reticulum ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Ischemic Injury ◽  
Calcium Overload ◽  
Mitochondrial Calcium ◽  
Myocardial Infarct Size ◽  
Hypoxic Injury

Our previous research has shown that type-2a Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2a) undergoes posttranscriptional oxidative modifications in cardiac microvascular endothelial cells (CMECs) in the context of excessive cardiac oxidative injury. However, whether SERCA2a inactivity induces cytosolic Ca2+ imbalance in mitochondrial homeostasis is far from clear. Mitofusin2 (Mfn2) is well known as an important protein involved in endoplasmic reticulum (ER)/mitochondrial Ca2+ tethering and the regulation of mitochondrial quality. Therefore, the aim of our study was to elucidate the specific mechanism of SERCA2a-mediated Ca2+ overload in the mitochondria via Mfn2 tethering and the survival rate of the heart under conditions of cardiac microvascular ischemic injury. In vitro, CMECs extracted from mice were subjected to 6 h of hypoxic injury to mimic ischemic heart injury. C57-WT and Mfn2KO mice were subjected to a 1 h ischemia procedure via ligation of the left anterior descending branch to establish an in vivo cardiac ischemic injury model. TTC staining, immunohistochemistry and echocardiography were used to assess the myocardial infarct size, microvascular damage, and heart function. In vitro, ischemic injury induced irreversible oxidative modification of SERCA2a, including sulfonylation at cysteine 674 and nitration at tyrosine 294/295, and inactivation of SERCA2a, which initiated calcium overload. In addition, ischemic injury-triggered [Ca2+]c overload and subsequent [Ca2+]m overload led to mPTP opening and ΔΨm dissipation compared with the control. Furthermore, ablation of Mfn2 alleviated SERCA2a-induced mitochondrial calcium overload and subsequent mito-apoptosis in the context of CMEC hypoxic injury. In vivo, compared with that in wild-type mice, the myocardial infarct size in Mfn2KO mice was significantly decreased. In addition, the findings revealed that Mfn2KO mice had better heart contractile function, decreased myocardial infarction indicators, and improved mitochondrial morphology. Taken together, the results of our study suggested that SERCA2a-dependent [Ca2+]c overload led to mitochondrial dysfunction and activation of Mfn2-mediated [Ca2+]m overload. Overexpression of SERCA2a or ablation of Mfn2 expression mitigated mitochondrial morphological and functional damage by modifying the SERCA2a/Ca2+-Mfn2 pathway. Overall, these pathways are promising therapeutic targets for acute cardiac microvascular ischemic injury.

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