Dataset Information

The Calmodulin/Striatin Interaction is Enhanced in Diabetic Hearts and Defines Novel Signaling Clusters implicated in Cardiac Remodeling

ABSTRACT: Diabetic cardiomyopathy (DbCM) halts cardiac performance with a complex etiology, hence the absence of an effective therapy for this disease. Herein we decoded the proteins hub interconnected with Calmodulin (CaM), a striatin (STRN) binding protein, that plays a role in DbCM. Using CaM as a bait, we precipitated protein clusters from left ventricles (LVs) of diabetic hearts at two stages of diabetes; 8- and 24-weeks rats treated with streptozotocin-STZ. Diabetic rats showed pathological heart remodeling confirmed by increased heart/body weight (HW/BW) ratio and increased β-MHC protein levels and ANF mRNA expression.

INSTRUMENT(S):

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Heart

DISEASE(S): Type 2 Diabetes Mellitus

SUBMITTER: Liaqat Ali

LAB HEAD: Moni Nader

PROVIDER: PXD069737 | Pride | 2026-06-15

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	030423_CaM_Fraction_.mzTab	Mztab
	030423_CaM_Fraction_1.mzML	Mzml
	030423_CaM_Fraction_1.raw	Raw
	030423_CaM_Fraction_2.mzML	Mzml
	030423_CaM_Fraction_2.raw	Raw

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The Calmodulin/Striatin Interaction Is Enhanced in Diabetic Hearts and Defines Novel Signaling Clusters Implicated in Cardiac Remodeling.

Chacar Stephanie S Al Hageh Cynthia C Ali Liaqat L Zalloua Pierre P Suleiman M-Saadeh MS Howarth Frank Christopher FC Khraibi Ali A AA Nader Moni M

ACS omega 20260518 21

Diabetic cardiomyopathy (DbCM) impairs cardiac performance through complex mechanisms, which limits effective therapies. We investigated the protein networks of calmodulin (CaM), a striatin (STRN)-binding protein implicated in DbCM, and compared them with the STRN network from the same tissues. Using CaM as bait, we precipitated protein clusters from left ventricles (LVs) of diabetic rat hearts at 8 and 24 weeks post-streptozotocin (post-STZ). Diabetic rats exhibited pathological remodeling, evi ...[more]

PMID: 42255577

Similar Datasets

Project description:OBJECTIVE: To study the genetic regulatory mechanisms in the remote zone of left ventricular (LV) free wall in order to partly explain the more frequent progression to heart failure after acute myocardial infarction (AMI) in diabetic rats. METHODS: 10 weeks after diabetes mellitus (DM) induction with Streptozotocin (STZ), the left anterior descending coronary arteries of uncontrolled diabetic Sprague-Dawley (SD) rats and non-diabetic ones were ligated without reperfusion. Then, the remote zone tissues of LV free wall were taken as samples at day 1, 7, 14, 28, and 56 post AMI. Significant different expression genes were filterd from Affymetrix Genechip U230 2.0 array by GCOS software. Genetic changes post myocardial infarction were classified by hierarchical clustering of 10 gene chips. And then, the differential expressions of 10 selected transcripts identified by the microarray were examined in greater detail by Real Time-PCR. RESULTS: According to hierarchical clustering, we find that the molecular regulatory expression related to cardiac remodeling in the remote zone to myocardial infarction is quite different as time elapses in both diabetic and non-diabetic rats. The gene expression at day 1 and 7 post AMI in both groups is similar, while the genetic changes at day 14 post AMI in diabetic rats and the ones at day 14 and 28 in non-diabetic rats are classified into the same cluster. And then the genetic changes at day 28 and 56 post AMI in diabetic rats and the ones at day 56 in non-diabetic rats are classified into the same cluster. (Figure.1) The patterns of numerous products of genes expression were used in the cluster, including 118 genes, such as leucine-rich PPR-motif containing (IL-6 signaling pathway), procollagen type I, VI, VIII, and XV, fibronectin1, RT1, and TIMP-1, etc. CONCLUSION: The genetic findings in this study might be the possible mechanism that diabetes mellitus can accerate the progression of post-infarction genetic regulatory expression. Experiment Overall Design: All studies were performed with male SD rats (200-220g), aged 8 weeks, which were obtained from laboratorial animal center of Chinese University of Agriculture. DM was induced with a singleintraperitoneal injection of STZ (65 mg/kg in 0.1mmol/L, pH 4.5 sodium citrate buffer) . Age and body weight matched rats that used as non-diabetic controls were injected with the same dose of sodium citrate buffer (0.1mmol/L, pH 4.5). Ultrastructure changes of myocardium were observed 10 weeks after DM induction by TEM. 10 weeks after DM induction,both diabetic and non-diabetic rats were subjected to left anterior descending coronary artery (LADCA) ischemia for 1-56 days without reperfusion. Two-dimensional echocardiography was utilized to obtain LV dimensions and LV percent fractional shortening at baseline, DM 10weeks, and at 1d, 7d, 14d, 28d, 56d after AMI; the remote zone tissues of LV free wall were taken as samples at day 1, 7, 14, 28, and 56 post AMI for gene chip microarray analysis (10 samples from 30 rats); in addition, heart-to-body weight and heart to tibial length ratios and masson's trichrome staining was measured as an index of cardiac hypertrophy and fibrosis at baseline, DM 10weeks, and at 1d, 7d, 14d, 28d, 56d after AMI.