Tropomyosin Isoforms in Nonmuscle Cells

Lin, Jim Jung‐Ching; Warren, Kerri S.; Wamboldt, Dawn D.; Wang, Tao; Lin, Jin-Lung

doi:10.1016/s0074-7696(08)61619-8

Cited by 148 publications

(121 citation statements)

References 215 publications

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“…In addition, colon mucosa of mice with DSSinduced colitis may be characterized by lower levels of microfilament-associated proteins tropomyosin 1 and 2 (Tpm1 and Tpm2), which are present in all eukaryotic cells with organ-specific isoforms having distinct functions (Lin et al, 1997). However, this downregulation of Tpm1 and Tpm2 induced by DSS was also ameliorated in mice administered SNE and PE.…”

Section: Continued) Differentially Expressed Proteins In the Colon Mmentioning

confidence: 99%

Preventive Effects of Spirogyra neglecta and a Polysaccharide Extract against Dextran Sodium Sulfate Induced Colitis in Mice

Taya

Kakehashi²,

Wongpoomchai³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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Ulcerative colitis (UC) results from colonic epithelial barrier defects and impaired mucosal immune responses. In this study, we aimed to investigate the modifying effects of a Spirogyra neglecta extract (SNE), a polysaccharide extract (PE) and a chloroform fraction (CF) on dextran sodium sulfate (DSS)-induced colitis in mice and to determine the mechanisms. To induce colitis, ICR mice received 3% DSS in their drinking water for 7 days. Seven days preceding the DSS treatment, oral administration of SNE, PE and CF at doses of 50, 25 and 0.25 mg/kg body weight (low dose), 200, 100 and 1 mg/kg body weight (high dose) and vehicle was started and continued for 14 days. Histologic findings showed that DSS-induced damage of colonic epithelial structure and inflammation was attenuated in mice pre-treated with SNE, PE and CF. Furthermore, SNE and PE significantly protected colonic epithelial cells from DSS-induced cell cycle arrest, while SNE, PE and CF significantly diminished apoptosis. Proteome analysis demonstrated that SNE and PE might ameliorate DSS-induced colitis by inducing antioxidant enzymes, restoring impaired mitochondria function, and regulating inflammatory cytokines, proliferation and apoptosis. These results suggest that SNE and PE could prevent DSS-induced colitis in ICR mice by protection against and/or aiding recovery from damage to the colonic epithelium, reducing ROS and maintaining normal mitochondrial function and apoptosis.

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Section: Continued) Differentially Expressed Proteins In the Colon Mmentioning

confidence: 99%

Preventive Effects of Spirogyra neglecta and a Polysaccharide Extract against Dextran Sodium Sulfate Induced Colitis in Mice

Taya

Kakehashi²,

Wongpoomchai³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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“…Colonies greater than 550 mm were counted and the quantitative data are shown in the upper panel (Prasad et al, 1993) transduction, and it is a suppressor of ras-transformed phenotype . In addition, interactions of TM1 with other TMs, as well as with other proteins such as caldesmon may prove to be important (Lin et al, 1997;Pittenger et al, 1994;Yamashiro et al, 1994).…”

Section: Growth Propertiesmentioning

confidence: 99%

“…Tropomyosins (TMs) are a family of important actin binding proteins which stabilize actin in the micro®laments (Lin et al, 1997;Pittenger et al, 1994). TMs are a-helical, rod-shaped proteins, classi®ed into high and low M r isoforms, consisting of 284 and 247 amino acids (aa), respectively.…”

mentioning

confidence: 99%

“…TM4 and TM5 (each with M r of 32 kDa) contain 247 aa and are described as low M r isoforms (Cooper et al, 1985;Prasad et al, 1993). The function of TMs in muscle cells, in conjunction with the troponins, as the components of actin-myosin contractile apparatus, is well-de®ned (Lin et al, 1997;Pittenger et al, 1994). However, in non-muscle cells the function(s) of TMs, given the tissue speci®c expression of multiple isoforms of TMs, coupled with the absence of troponin complex, is largely unknown; also, it is unclear whether each of the isoforms performs any unique cell type speci®c functions.…”

mentioning

confidence: 99%

“…However, in non-muscle cells the function(s) of TMs, given the tissue speci®c expression of multiple isoforms of TMs, coupled with the absence of troponin complex, is largely unknown; also, it is unclear whether each of the isoforms performs any unique cell type speci®c functions. Recent ®ndings from several laboratories suggest that the individual TMs may perform speci®c, as well as overlapping functions in the cell (reviewed in Lin et al, 1997;Pittenger et al, 1994).…”

mentioning

confidence: 99%

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Suppression of src-induced transformed phenotype by expression of tropomyosin-1

et al. 1999

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Suppression of high M r tropomyosins (TMs) is a common feature of transformed cells. Previous work from this laboratory has demonstrated that the isoform 1 of TM, TM1, acts as an anti-oncogene in rastransformed murine ®broblasts. In this study, we have investigated whether TM1 is a ras-speci®c suppressor, or a general suppressor protein of the cellular transformation. V-src transformed ®broblasts, which express decreased TM1, were transduced with a full-length cDNA to overexpress TM1. Both the control and the transduced cells expressed v-src kinase at comparable levels. TM1 expressing (src-T1) cells grew at a lower rate in monolayer, exhibited well spread,¯at morphology than the control cells. Enhanced expression of TM1 resulted in improved micro®lamental architecture. More signi®cantly, src-T1 cells completely failed to grow under anchorage independent conditions. These data demonstrate that TM1 is as an anti-oncogene of functionally diverse oncogenes, and it is a class II tumor suppressor protein.

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