Tomato is a model species for fleshy fruit development. The shapes and sizes of tomato (Solanum lycopersicum L.) are mainly controlled by several loci, including locule number (lc). Two single nucleotide polymorphisms were found downstream of WUSCHEL (SlWUS) in a putative tomato CArG cis-regulatory element. The lc mutation may affect the binding of AGAMOUS(AG), cause the up-regulation of SlWUS and result in increased locule numbers. In this study, tissue expression levels showed that SlWUS is expressed in young floral buds and shoot apexes. Silencing SlWUS on an lc mutant genetic background with an RNA interference (RNAi) strategy resulted in smaller flowers and fruit than those of the wild-type plants, with decreased locule number. Further study revealed that the SlWUS RNAi lines exhibited altered expression levels of the TAG1 and SlCLV3 genes that participate in the regulation of tomato flower and fruit locule development. In conclusion, this study provides the first genetic evidence that SlWUS may be the candidate gene of the lc locus and reveals the function of SlWUS in flower development.

Extensive investigations into long noncoding RNAs (lncRNAs) in various diseases and cancers, including acute myocardial infarction (AMI) have been conducted. The current study aimed to investigate the role of lncRNA solute carrier family 8 member A1 antisense RNA 1 (SLC8A1‐AS1) in myocardial damage by targeting solute carrier family 8 member A1 (SLC8A1) via cyclic guanosine 3′,5′‐monophosphate‐protein kinase G (cGMP‐PKG) signaling pathway in AMI mouse models. Differentially expressed lncRNA in AMI were initially screened and target relationship between lncRNA SLC8A1‐AS1 and SLC8A1 was then verified. Infarct size, levels of inflammatory factors, biochemical indicators, and the positive expression of the SLC8A1 protein in AMI were subsequently determined. The expression of SLC8A1‐AS1, SLC8A1, PKG1, PKG2, atrial natriuretic peptide, and brain natriuretic peptide was detected to assess the effect of SLC8A1‐AS1 on SLC8A1 and cGMP‐PKG. The respective contents of superoxide dismutase, lactate dehydrogenase (LDH), and malondialdehyde (MDA) were detected accordingly. Microarray data GSE66360 provided evidence indicating that SLC8A1‐AS1 was poorly expressed in AMI. SLC8A1 was verified to be a target gene of lncRNA SLC8A1‐AS1. SLC8A1‐AS1 upregulation decreased levels of left ventricular end‐systolic diameter, −dp/ dt max, interleukin 1β (IL‐1β), IL‐6, transforming growth factor α, nitric oxide, inducible nitric‐oxide synthase, endothelial nitric‐oxide synthase, infarct size, LDH activity and MDA content, and increased IL‐10, left ventricular end‐diastolic pressure and + dp/ dt max. Furthermore, the overexpression of SLC8A1‐AS1 was noted to elicit an inhibitory effect on the cGMP‐PKG signaling pathway via SLC8A1. In conclusion, lncRNA SLC8A1‐AS1, by downregulating SLC8A1 and activating the cGMP‐PKG signaling pathway, was observed to alleviate myocardial damage, inhibit the release of proinflammatory factors and reduce infarct size, ultimately protecting against myocardial damage.

Necrotizing enterocolitis (NEC) is an acute intestinal condition accounting for severe mortality and morbidity in preterm infants. This study aimed to identify the possible roles of let-7d-5p in neonatal rats with NEC. The differentially expressed genes (DEGs) related to NEC were initially screened in silico. After establishment of NEC rat models, the measurement of the expression of let-7d-5p, galectin-3 (LGALS3), toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-κB) as well as proinflammatory cytokines (TNF-α, IL-1b and IL-6) was conducted. The interaction between let-7d-5p and LGALS3 or Argonaute2 (AGO2) was identified. Gain- and loss-function approaches were then performed in an attempt to investigate the regulatory roles of let-7d-5p and LGALS3 in inflammation and cell apoptosis in NEC neonatal rats. Let-7d-5p was poorly expressed, while LGALS3, TLR4 and NF-κB were highly expressed in the intestinal tissues of NEC rats. Over-expression of let-7d-5p resulted in decreased levels of proinflammatory factors in the intestinal tissues of NEC rats. Through sequential experimentation, let-7d-5p was identified to target LGALS3 and bind to AGO2. In addition, LGALS3 silencing or LPS treatment blocked the TLR4/NF-κB signaling pathway, thereby suppressing intestinal epithelial cell apoptosis and inflammation in NEC. Collectively, let-7d-5p might exercise its inhibitory properties in the inflammatory response and intestinal epithelial cell apoptosis in NEC neonatal rats via inactivation of the LGALS3-dependent TLR4/NF-κB signaling pathway.

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Recent studies have shown that circulating microRNAs (miRNA) play a critical role in diagnosing acute coronary syndrome (ACS). This study aims to investigate the effect of miR‐224 on atherosclerotic plaques forming and vascular remodeling in ACS and its relationship with TGF‐β/Smad pathway. Myocardial infarction (MI) rat model was established and lentivirus vector of miR‐224 inhibitor was prepared for investigating the effect of downregulated miR‐224 on the contents of nitric oxide (NO) and endothelin‐1 (ET‐1), blood lipid levels and inflammatory factor levels in serum as well as the TGF‐β/Smad pathway. The rats suffering from MI had decreased survival rates and exhibited reduced levels of NO, high‐density lipoprotein cholesterol, and lumen diameter, and Smad7 messenger RNA (mRNA) and protein expression; while had significantly increased ratio of heart weight or body weight, levels of ET‐1, inflammatory factors, blood lipid indexes, vascular remodeling indexes, collagen volume fraction, vulnerable atherosclerotic plaque area, VCAM‐1 and MMP‐2 protein expression, TGF‐β, Smad2, Smad3, and Smad4 mRNA and protein expression. After inhibiting the TGF‐β/Smad pathway, the rats suffering from MI showed notably opposite trend. In conclusion, downregulation of miR‐224 expression promotes the formation of vulnerable atherosclerotic plaques and vascular remodeling in ACS through activation of the TGF‐β/Smad pathway. Therefore, this study provides a new therapeutic target for ACS.