Journal of Pathology and Translational Medicine

Original Articles

The Expression of Transforming Growth Factor-beta1 and alpha-Smooth Muscle Actin is Increased in the Human Myxomatous Valve.: Jeong Hwan Park, Ho Joong Youn, Jung Sook Yoon, Chul Soo Park, Soo Sung Oh, Woo Baek Chung, Jong Won Chung, Yun Seok Choi, Dong Hyun Lee, Yong Seog Oh, Wook Sung Chung, Soon Jo Hong, Youn Soo Lee, Sung Bo Sim, Sun Hee Lee; Korean J Pathol. 2009;43(2):152-156.; DOI: https://doi.org/10.4132/KoreanJPathol.2009.43.2.152

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BACKGROUND
In vitro experimental studies have reported that transforming growth factor-beta1 (TGF-beta1) stimulates the production of alpha-smooth muscle actin (alpha-SMA) in porcine valves. However, the relation between TGF-beta1 and alpha-SMA in myxomatous valves has not been elucidated.
METHODS
We classified 27 subjects into two groups: 1) myxomatous group (M:F=11:12, mean age=55+/-15 years) and 2) rheumatic group (M:F=3:1, mean age=41+/-17 years) according to preoperative echocardiographic and postoperative histologic findings. Twenty-seven valve specimens from the patients who underwent valve replacement were obtained. Tissue samples were analyzed by immunohistochemistry for TGF-beta1 and alpha-SMA. The positively stained areas were measured using an image analysis program (Image Pro-Plus 4.5), and then the TGF-beta1 volume fraction (TGF-VF) and alpha-SMA volume fraction (alpha-SMA-VF) were calculated.
RESULTS
TGF-VF in myxomatous valves was higher than in rheumatic valves (2,759+/-2,294 vs 864+/-276, p=0.04). alpha-SMA-VF in myxomatous valves was higher than in rheumatic valves (4,122+/-2,275 vs 2,421+/-844, p=0.002). There was a significant correlation between TGF-beta1 and alpha-SMA in myxomatous valves (r=0.38, p=0.04). There was no significant correlation between TGF-beta1 and alpha-SMA in rheumatic valves (r=-0.50, p=0.67).
CONCLUSIONS
TGF-beta1 and alpha-SMA may be related to the pathogenesis of myxomatous valves. The activation of TGF-beta1 might increase the expression of alpha-SMA in human myxomatous valves.

Citations

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Apoptosis and abundance of Bcl-2 family and transforming growth factor β1 signaling proteins in canine myxomatous mitral valves
Sirilak Surachetpong, Treenate Jiranantasak, Anudep Rungsipipat, E. Christopher Orton
Journal of Veterinary Cardiology.2013; 15(3): 171. CrossRef
Pathology, protein expression and signaling in myxomatous mitral valve degeneration: Comparison of dogs and humans
Heike Aupperle, Sirilak Disatian
Journal of Veterinary Cardiology.2012; 14(1): 59. CrossRef

Expression of TGF-beta1 Protein in Macrophages of Tuberculous Granulomas.: Jong Im Lee, Jung Ran Kim, Tae Jung Jang, Dong Hoon Kim; Korean J Pathol. 1998;32(4):261-265.

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Abstract PDF: TGF-beta1 expression was studied in 25 patients with tuberculosis (lung, 9 cases and lymph node, 16 cases) using a polyclonal antibody in formalin-fixed paraffin embedded tissue. Nineteen cases (76.0%) out of 25 cases showed TGF-beta1 expression. TGF-beta1 was present in cytoplasm of epithelioid cells and Langhans' giant cells. Pulmonary tuberculosis and tuberculous lymphadenitis showed different patterns of staining. Five of 9 cases of pulmonary tuberculosis were positive for TGF-beta1: four of acid-fast bacilli positive cases (4/5, 80.0%) and one of acid-fast bacilli negative cases (1/4, 25.0%). However, high expression of TGF-beta1 was detected in tuberculous lymphadenitis of both acid-fast bacilli positive group (3/4, 75.0%) and acid-fast bacilli negative group (11/12, 91.7%). TGF-beta1 was also expressed in all of 6 cases of BCG-induced tuberculous lymphadenitis: 2 acid-fast bacilli positive and 4 acid-fast bacilli negative cases. TGF-beta1 expression was shown in 19 cases (86.4%) of 22 in active tuberculosis, while no TGF-beta1 expression was detected in any cases of inactive, healed tuberculosis (p<0.008). This study supports that the TGF-beta1 expression of epithelioid cells may alter their function resulting in the impaired antimycobacterial activity. Thus the increased production of TGF-beta1 may be one of the important mechanisms by which Mycobacterium tuberculosis avoids destruction by host macrophages.

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