Heart failure is the leading cause of combined morbidity and mortality in the USA with 50% of cases being diastolic heart failure. Diastolic heart failure results from poor myocardial relaxation and inadequate filling of the left ventricular chamber caused in part by calcium-handling dysregulation. In this chapter we describe methods to investigate new approaches of novel human Ca 2+ binding protein motifs to restore normal Ca 2+ handling function to diseased myocardium. Gene transfer of parvalbumin into adult cardiac myocytes has been studied as a potential therapeutic, specifically as a strategic Ca 2+ buffer to correct cardiac mechanical dysfunction in disease. This chapter provides protocols for studying wild-type parvalbumin isoforms and parvalbumins with strategically designed EF-hand motifs in adult cardiac myocytes via acute adenoviral gene transfer. These protocols have been used extensively to optimize parvalbumin function as a potential therapeutic for failing heart muscle.
|Original language||English (US)|
|Title of host publication||Methods in Molecular Biology|
|Publisher||Humana Press Inc.|
|Number of pages||19|
|State||Published - 2019|
|Name||Methods in Molecular Biology|
Bibliographical noteFunding Information:
This work was supported by funds from NIH.
- Adult cardiac myocyte
- Calcium imaging
- Gene transfer
PubMed: MeSH publication types
- Journal Article
- Research Support, N.I.H., Extramural