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Int J Physiol Pathophysiol Pharmacol 2010;2(1):12-19.
Original Article
Sm22α transcription occurs at the early onset of the cardiovascular system and the
intron I is dispensable for its transcription in smooth muscle cells during mouse
development
Maozhou Yang, Hong Jiang, Li Li
Dept of Internal Medicine, Wayne State University, Detroit MI 48201, USA; Center for Molecular Medicine and Genetics, Wayne State
University, Detroit, MI 48201, USA; Cardiovascular Research Institute, Wayne State University, Detroit, MI 48201, USA; Bone and Joint
Center, Henry Ford Hospital, 2799 West Grand Blvd., Detroit, MI 48202, USA
Received November 11, 2009; accepted November, 2009; available online November, 2009
Abstract: SM22α, also known as SM22, has been widely used as a smooth muscle cells (SMC) marker and is known to be expressed
in the embryonic heart. The intron I of Sm22 contains multiple important evolutionarily conserved regulatory elements. To determine the
role of the intron I in Sm22 transcriptional regulation and the function of SM22 during development, we generated a Sm22 knockout
mouse by replacing the intron I and the translation initiation with a nuclear localized LacZ (nLacZ) reporter. The resulting Sm22
knockout mice (sm22-/-) were viable and fertile without any apparent developmental defects. Using X-gal staining assay, we found that
Sm22 transcription was detectable in the chorion formation region and in the heart field before formation of the heart tube at E7.5,
namely much earlier than the looped heart stage where it had been previously reported. The expression of lacZ progressively expanded
throughout the heart tube by E8.5. LacZ was transiently expressed in the heart and somites and then became restricted to the vascular
and visceral SMC organs. These results indicate that SM22 is not required for mouse basal homeostatic function and that the intron I is
dispensable for Sm22 transcription during development. Given the importance of vasculature in organogenesis and in diseases, this
mouse line may be a valuable tool to trace the development and pathology of the cardiovascular system. (IJPPP911003).
Key words: SM22α, Transgelin, smooth muscle cells, intron I, knockout mouse, cardiac crescent
Full Text PDF
Address all correspondence to:
Li Li, PhD
Dept of Internal Medicine, Wayne State University
421 E. Canfield Ave. Room #1107, Detroit MI 48201.
TEL: 313-577-8749
FAX: 313-577-8615
Email: lili@med.wayne.edu.
Original Article
Sm22α transcription occurs at the early onset of the cardiovascular system and the
intron I is dispensable for its transcription in smooth muscle cells during mouse
development
Maozhou Yang, Hong Jiang, Li Li
Dept of Internal Medicine, Wayne State University, Detroit MI 48201, USA; Center for Molecular Medicine and Genetics, Wayne State
University, Detroit, MI 48201, USA; Cardiovascular Research Institute, Wayne State University, Detroit, MI 48201, USA; Bone and Joint
Center, Henry Ford Hospital, 2799 West Grand Blvd., Detroit, MI 48202, USA
Received November 11, 2009; accepted November, 2009; available online November, 2009
Abstract: SM22α, also known as SM22, has been widely used as a smooth muscle cells (SMC) marker and is known to be expressed
in the embryonic heart. The intron I of Sm22 contains multiple important evolutionarily conserved regulatory elements. To determine the
role of the intron I in Sm22 transcriptional regulation and the function of SM22 during development, we generated a Sm22 knockout
mouse by replacing the intron I and the translation initiation with a nuclear localized LacZ (nLacZ) reporter. The resulting Sm22
knockout mice (sm22-/-) were viable and fertile without any apparent developmental defects. Using X-gal staining assay, we found that
Sm22 transcription was detectable in the chorion formation region and in the heart field before formation of the heart tube at E7.5,
namely much earlier than the looped heart stage where it had been previously reported. The expression of lacZ progressively expanded
throughout the heart tube by E8.5. LacZ was transiently expressed in the heart and somites and then became restricted to the vascular
and visceral SMC organs. These results indicate that SM22 is not required for mouse basal homeostatic function and that the intron I is
dispensable for Sm22 transcription during development. Given the importance of vasculature in organogenesis and in diseases, this
mouse line may be a valuable tool to trace the development and pathology of the cardiovascular system. (IJPPP911003).
Key words: SM22α, Transgelin, smooth muscle cells, intron I, knockout mouse, cardiac crescent
Full Text PDF
Address all correspondence to:
Li Li, PhD
Dept of Internal Medicine, Wayne State University
421 E. Canfield Ave. Room #1107, Detroit MI 48201.
TEL: 313-577-8749
FAX: 313-577-8615
Email: lili@med.wayne.edu.
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