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New mouse models enable precise targeting of smooth muscle cells (SMCs), distinguishing between arterial and nonvascular subtypes. This advancement allows for detailed study of SMC roles in various organs and diseases, particularly pulmonary arterial hypertension.

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Area of Science:

  • Genetics and Genomics
  • Cardiovascular Biology
  • Cell Biology

Background:

  • Current Cre/loxP systems lack specificity for smooth muscle cell (SMC) subtypes, hindering targeted gene manipulation.
  • Existing mouse lines exhibit off-target activity, complicating studies of arterial SMCs (ASMCs) and nonvascular SMCs (NVSMCs).
  • Precise genetic tools are crucial for understanding SMC functions in diverse physiological and pathological contexts.

Purpose of the Study:

  • To develop novel mouse lines for highly specific targeting of ASMCs and NVSMCs.
  • To investigate organ-specific transcriptomic differences in ASMCs and NVSMCs.
  • To assess the functional impact of SMC-specific gene manipulation in disease models.

Main Methods:

  • Generation of a novel mouse line combining Cspg4-Dre and Acta2-rox-CreER for exclusive ASMC targeting.
  • Utilized Chrm2-Dre and Acta2-rox-CreER for specific NVSMC targeting.
  • Employed RNA sequencing and fluorescence-activated cell sorting for transcriptomic profiling.
  • Assessed gene function via inactivation of RBPMS and RBPMS2 in SMCs.

Main Results:

  • Achieved exclusive Cre activity in ASMCs using the Cspg4-Dre/Acta2-rox-CreER system.
  • Demonstrated specific targeting of NVSMCs with the Chrm2-Dre/Acta2-rox-CreER combination.
  • Revealed distinct transcriptomic signatures in ASMCs across different organs.
  • Identified organ-specific transcriptional variations in NVSMCs.
  • Observed altered pulmonary artery structure upon RBPMS/RBPMS2 inactivation in ASMCs.
  • Demonstrated loss of NVSMC contractility in the intestine following inactivation in all SMCs.

Conclusions:

  • Developed highly specific mouse lines for targeting ASMCs and NVSMCs, enabling distinction between vascular and nonvascular SMC functions.
  • Identified vessel bed-specific gene signatures, facilitating targeted SMC manipulation in diseases like pulmonary arterial hypertension.
  • These tools advance the study of SMCs in organ-specific diseases and physiological processes.