The effect of the plant hormone indole-3-acetic acid and chemically related compounds on the growth of mouse fibroblast 3t3 cells

Sinna, G. Abu

doi:10.1016/0742-8413(83)90127-5

Cited by 4 publications

(5 citation statements)

References 11 publications

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“…IAA regulates growth and essential for plant’s life cycle and body development. In addition, IAA increased the growth of mouse and human fibroblasts 24 . We recently found that MA-35 showed anti-TNF-α activity mediated by inhibiting IκB kinase (IKK) phosphorylation, which attenuated the hepatic and renal inflammation in the mice 25 .…”

Section: Introductionmentioning

confidence: 96%

The indole compound MA-35 attenuates tumorigenesis in an inflammation-induced colon cancer model

Kanehara

Ohnuma

Kanazawa

et al. 2019

Sci Rep

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In inflammatory bowel disease, chronic inflammation results in the development of colon cancer known as colitis-associated cancer. This disease is associated with tumor necrosis factor-α (TNF-α) signaling. In addition, intestinal fibrosis is a common clinical complication that is promoted by transforming growth factor β1 (TGF-β 1 ). In our previous study, MA-35 attenuated renal fibrosis by inhibiting both TNF-α and TGF-β 1 signaling. This study aimed to identify the possible antitumor effects and antifibrotic effects of MA-35 using an AOM/DSS mouse model. MA-35 was orally administered every day for 70 days in the AOM/DSS mouse model. There was no difference in weight loss between the AOM/DSS group and the AOMDSS + MA-35 group, but the disease activity index score and the survival rate were improved by MA-35. MA-35 blocked the anemia and shortening of the colon induced by AOM/DSS. MA-35 reduced the macroscopic formation of tumors in the colon. In the microscopic evaluation, MA-35 reduced inflammation and fibrosis in areas with dysplasia. Furthermore, the TNF-α mRNA level in the colon tended to be reduced, and the interleukin 6, TGF-β 1 and fibronectin 1 mRNA levels in the colon were significantly reduced by MA-35. These results suggested that MA-35 inhibited AOM/DSS-induced carcinogenesis by reducing inflammation and fibrosis.

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Section: Introductionmentioning

confidence: 96%

The indole compound MA-35 attenuates tumorigenesis in an inflammation-induced colon cancer model

Kanehara

Ohnuma

Kanazawa

et al. 2019

Sci Rep

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“…IAA also increased the growth of mouse and human fibroblasts (Abu Sinna 1983). To identify the potential drugs for stimulating cell survival, we screened the inhouse chemical library of IAA analogs (Hayashi et al 2012) based on the increase of the cellular ATP contents compared with the control.…”

Section: Screening For Iaa Derivatives That Increase Cellular Atp Levelsmentioning

confidence: 99%

“…IAA regulates growth and essential for plant's life cycle and body development, but IAA is synthesized in the mouse liver and kidney (Gordon et al 1972) and intestinal anaerobes (Chung et al 1975). In addition, IAA increased the growth of mouse and human fibroblasts (Abu Sinna 1983), although the precise role and mechanism has not been clarified. We are therefore interested in the bioactive properties of IAA.…”

Section: Introductionmentioning

confidence: 99%

Mitochonic Acid 5 (MA-5), a Derivative of the Plant Hormone Indole-3-Acetic Acid, Improves Survival of Fibroblasts from Patients with Mitochondrial Diseases

Suzuki

Yamaguchi

Kikusato

et al. 2015

Tohoku J. Exp. Med.

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Mitochondria are key organelles implicated in a variety of processes related to energy and free radical generation, the regulation of apoptosis, and various signaling pathways. Mitochondrial dysfunction increases cellular oxidative stress and depletes ATP in a variety of inherited mitochondrial diseases and also in many other metabolic and neurodegenerative diseases. Mitochondrial diseases are characterized by the dysfunction of the mitochondrial respiratory chain, caused by mutations in the genes encoded by either nuclear DNA or mitochondrial DNA. We have hypothesized that chemicals that increase the cellular ATP levels may ameliorate the mitochondrial dysfunction seen in mitochondrial diseases. To search for the potential drugs for mitochondrial diseases, we screened an in-house chemical library of indole-3-acetic-acid analogs by measuring the cellular ATP levels in Hep3B human hepatocellular carcinoma cells. We have thus identified mitochonic acid 5 (MA-5), 4-(2,4-difluorophenyl)-2-(1H-indol-3-yl)-4-oxobutanoic acid, as a potential drug for enhancing ATP production. MA-5 is a newly synthesized derivative of the plant hormone, T. Suzuki et al. 226

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“…It also accumulates in human renal failure 6 . Additionally, IAA also promotes fibroblast proliferation in both mice and humans 7 . Recent research has even demonstrated that microbiota-derived IAA enhances the effectiveness of chemotherapy in pancreatic ductal adenocarcinoma 8 .…”

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confidence: 99%

Mitochonic acid 5 attenuates age-related neuromuscular dysfunction associated with mitochondrial Ca2+ overload in Caenorhabditis elegans

Seida

Abe

et al. 2023

npj Aging

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Mitochonic acid-5 ameliorates the pathophysiology of human mitochondrial-disease fibroblasts and Caenorhabditis elegans Duchenne muscular dystrophy and Parkinson’s disease models. Here, we found that 10 μM MA-5 attenuates the age-related decline in motor performance, loss of muscle mitochondria, and degeneration of dopaminergic neurons associated with mitochondrial Ca2+ overload in C. elegans. These findings suggest that MA-5 may act as an anti-aging agent against a wide range of neuromuscular dysfunctions in metazoans.

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The effect of the plant hormone indole-3-acetic acid and chemically related compounds on the growth of mouse fibroblast 3t3 cells

Cited by 4 publications

References 11 publications

The indole compound MA-35 attenuates tumorigenesis in an inflammation-induced colon cancer model

The indole compound MA-35 attenuates tumorigenesis in an inflammation-induced colon cancer model

Mitochonic Acid 5 (MA-5), a Derivative of the Plant Hormone Indole-3-Acetic Acid, Improves Survival of Fibroblasts from Patients with Mitochondrial Diseases

Mitochonic acid 5 attenuates age-related neuromuscular dysfunction associated with mitochondrial Ca2+ overload in Caenorhabditis elegans

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