Antagonistic reactions of arginine and lysine against formaldehyde and their relation to cell proliferation, apoptosis, folate cycle and photosynthesis

2003 ◽  
pp. 167-176 ◽  
Author(s):  
Lajos Trézl ◽  
Lehel Hullán ◽  
Zsuzsa M. Jászay ◽  
Tibor Szarvas ◽  
Imre Petneházy ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Folate Cycle

scholarly journals MiR-22, regulated by MeCP2, suppresses gastric cancer cell proliferation by inducing a deficiency in endogenous S-adenosylmethionine

Oncogenesis ◽  
2020 ◽  
Vol 9 (11) ◽  
Author(s):  
Dongdong Tong ◽  
Jing Zhang ◽  
Xiaofei Wang ◽  
Qian Li ◽  
Liying Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Metabolic Pathways ◽  
Gastric Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Distal Enhancer ◽  
Methyl Donor ◽  
Cell Cycle Transition ◽  
Gastric Cancer Cell Proliferation ◽  
Folate Cycle

Abstract This study investigated the effect of methyl-CpG-binding protein 2 (MeCP2) on miRNA transcription. Our results of miRNA chip assay and ChIP-seq showed that MeCP2 inhibited the expressions of numerous miRNAs by binding to their upstream elements, including not only the promoter but also the distal enhancer. Among the affected miRNAs, miR-22 was identified to remarkably suppress gastric cancer (GC) cell proliferation, arrest G1–S cell cycle transition, and induce cell apoptosis by targeting MeCP2, MTHFD2, and MTHFR. Understanding GC metabolism characteristics is the key to developing novel therapies that target GC metabolic pathways. Our study revealed that the metabolic profiles in GC tissues were altered. SAM (S-adenosylmethionine), a universal methyl donor for histone and DNA methylation, which is specifically involved in the epigenetic maintenance of cancer cells, was found increased. The production of SAM is promoted by the folate cycle. Knockdown of MTHFD2 and MTHFR, two key enzymes in folate metabolism and methyl donor SAM production, significantly suppressed GC cell proliferation. MiR-22 overexpression reduced the level of endogenous SAM by suppressing MTHFD2 and MTHFR, inducing P16, PTEN, and RASSF1A hypomethylation. In conclusion, our study suggests that miR-22 was inhibited by MeCP2, resulting in deficiency of endogenous SAM, and ultimately leading to tumor suppressor dysregulation.

Fibroblasts During Hypertrophic Scar Formation and Resolution

1973 ◽  
Vol 31 ◽  
pp. 428-429
Author(s):  
C. W. Kischer
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Cell Proliferation ◽  
Fine Structure ◽  
Metabolic Activity ◽  
Hypertrophic Scar ◽  
Normal Skin ◽  
Ground Substance ◽  
Hypertrophic Scars ◽  
Scanning Electron

The morphology of the fibroblasts changes markedly as the healing period from burn wounds progresses, through development of the hypertrophic scar, to resolution of the scar by a self-limiting process of maturation or therapeutic resolution. In addition, hypertrophic scars contain an increased cell proliferation largely made up of fibroblasts. This tremendous population of fibroblasts seems congruous with the abundance of collagen and ground substance. The fine structure of these cells should reflect some aspects of the metabolic activity necessary for production of the scar, and might presage the stage of maturation.A comparison of the fine structure of the fibroblasts from normal skin, different scar types, and granulation tissue has been made by transmission (TEM) and scanning electron microscopy (SEM).

The Effect of Androgen Depletion and Replacement on the Epithelium of the Seminal Vesicle of the Aging Rat

1975 ◽  
Vol 33 ◽  
pp. 590-591
Author(s):  
Venita F. Allison
Keyword(s):  
Cell Proliferation ◽  
Seminal Vesicle ◽  
Male Rats ◽  
Target Cells ◽  
Cell Regeneration ◽  
Secretory Function ◽  
Electron Microscopic ◽  
Aging Rat ◽  
Microscopic Studies ◽  
Androgen Depletion

In 1930, Moore, Hughes and Gallager reported that after castration seminal vesicle epithelial cell atrophy occurred and that cell regeneration could be achieved with daily injections of testis extract. Electron microscopic studies have confirmed those observations and have shown that testosterone injections restore the epithelium of the seminal vesicle in adult castrated male rats. Studies concerned with the metabolism of androgens point out that dihydrotestosterone stimulates cell proliferation and that other metabolites of testosterone probably influence secretory function in certain target cells.Although the influence of androgens on adult seminal vesicle epithelial cytology is well documented, little is known of the effect of androgen depletion and replacement on those cells in aging animals. The present study is concerned with the effect of castration and testosterone injection on the epithelium of the seminal vesicle of aging rats.

Acetaminophen: Macula densa hypersecretory activity by induced hepatotoxicity

1987 ◽  
Vol 45 ◽  
pp. 934-935
Author(s):  
S.S. Poolsawat ◽  
C.A. Huerta ◽  
S.TY. Lae ◽  
G.A. Miranda
Keyword(s):  
Cell Proliferation ◽  
Liver Function ◽  
Chronic Inflammation ◽  
Foam Cell ◽  
Term Effect ◽  
Short Term ◽  
Drug Induced ◽  
Experimental Induction ◽  
Tissue Alterations ◽  
Toxic Responses

Introduction. Experimental induction of altered histology by chemical toxins is of particular importance if its outcome resembles histopathological phenomena. Hepatotoxic drugs and chemicals are agents that can be converted by the liver into various metabolites which consequently evoke toxic responses. Very often, these drugs are intentionally administered to resolve an illness unrelated to liver function. Because of hepatic detoxification, the resulting metabolites are suggested to be integrated into the macromolecular processes of liver function and cause an array of cellular and tissue alterations, such as increased cytoplasmic lysis, centrilobular and localized necroses, chronic inflammation and “foam cell” proliferation of the hepatic sinusoids (1-4).Most experimentally drug-induced toxicity studies have concentrated primarily on the hepatic response, frequently overlooking other physiological phenomena which are directly related to liver function. Categorically, many studies have been short-term effect investigations which seldom have followed up the complications to other tissues and organs when the liver has failed to function normally.

Cdh1, the anaphase promoting complex or cyclosome (APC/C) cofactor, inhibits trophoblast cell proliferation and invasion

2010 ◽  
Vol 34 (8) ◽  
pp. S10-S10
Author(s):  
Baoping Zhang ◽  
Jing Peng ◽  
Li Zhang ◽  
Hong Xu ◽  
Haibin Kuang
Keyword(s):  
Cell Proliferation ◽  
Trophoblast Cell ◽  
Anaphase Promoting Complex ◽  
Proliferation And Invasion

EMBJ08, a novel gene promoting cell proliferation

2010 ◽  
Vol 34 (8) ◽  
pp. S50-S50
Author(s):  
Jing Li ◽  
Dongxia Hao ◽  
Weiwei Deng ◽  
Na Li ◽  
Shai Guo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Novel Gene

HAb18G/CD147 enhances cell proliferation by promoting G0/G1 to S transition by ERK1/2 dependent cyclin D1 synthesis in human hepatoma cells

2010 ◽  
Vol 34 (8) ◽  
pp. S45-S45
Author(s):  
Yunshan Guo ◽  
Juan Tang ◽  
Zhinan Chenand Jianli Jiang
Keyword(s):  
Cell Proliferation ◽  
Cyclin D1 ◽  
Hepatoma Cells ◽  
Human Hepatoma ◽  
Human Hepatoma Cells

ACE INHIBITION ATTENUATES RENAL PDGF GENE EXPRESSION AND CELL PROLIFERATION IN SUBTOTAL NEPHRECTOMY

Nephrology ◽  
2000 ◽  
Vol 5 (3) ◽  
pp. A104-A104
Author(s):  
Jandeleit‐Dahm K ◽  
Wu Ll ◽  
Johnson Rj ◽  
Cox Aj ◽  
Kelly Dj ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Ace Inhibition ◽  
Subtotal Nephrectomy

Cyste(i)ne stimulates intestinal cell proliferation independent of glutathione synthesis

2001 ◽  
Vol 120 (5) ◽  
pp. A502-A502
Author(s):  
T NODA ◽  
R IWAKIRI ◽  
K FUJIMOTO ◽  
T AW
Keyword(s):  
Cell Proliferation ◽  
Intestinal Cell ◽  
Glutathione Synthesis

Involvement of tumor necrosis factor αin intestinal epithelial cell proliferation following paneth cell destruction

2001 ◽  
Vol 120 (5) ◽  
pp. A501-A501
Author(s):  
H SENO ◽  
M SAWADA ◽  
T KAYAHARA ◽  
H FUKUZAWA ◽  
Y FUJISAWA ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Necrosis Factor ◽  
Epithelial Cell ◽  
Tumor Necrosis ◽  
Intestinal Epithelial Cell ◽  
Paneth Cell ◽  
Intestinal Epithelial ◽  
Epithelial Cell Proliferation ◽  
Cell Destruction ◽  
Necrosis Factor
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