Effects of shRNA‑mediated silencing of PDE5A3 on intracellular cGMP and free Ca²⁺ levels and human prostate smooth muscle cell proliferation from benign prostatic hyperplasia

Comparative RNA-sequencing analysis of the prostate in a mouse model of benign prostatic hyperplasia with bladder outlet obstruction

“…By RNA-seq, 833 signi cantly differentially expressed genes were identi ed between the two groups. In the results of GO enrichment analysis, we found that up-regulated DEGs were signi cantly enriched in redox, which was consistent with previous studies that the redox system was associated with the development of BPH 43 , and that GO terms enriched in down-regulated DEGs were associated with ion transport 44 , whereas up down-regulated DEGs were enriched in hormonal regulation, and previous studies had demonstrated the involvement of both androgens and estrogens in the progression of BPH 45,46 . In addition, the results of KEGG analysis suggested that the most signi cant pathway was small molecules, which had been shown in previous studies to in uence cell cycle, apoptosis, proliferation, and proliferation [47][48][49] , whereas the up-regulated DEGs were most signi cantly enriched in pathways associated with IGFs and IGFBPs, which have been previously shown to be associated with BPH 50,51 , and inhibition of IGF-1 secretion inhibited the proliferation of prostate epithelial cells 52 , and up-and down-regulated DEGs were also predominantly co-enriched in small molecule compound-related pathways, suggesting that this pathway might play an important role in steroid hormones-induced BPH.…”

A 2‐week treatment with 5‐azacytidine improved the hypercontractility state in prostate from obese mice: Role of the nitric oxide‐cyclic guanosine monophosphate signalling pathway

“…Although the anatomy of prostate from rodents differs from that of humans, 15 several physiological pathways including the adrenergic, purinergic, cholinergic and NO‐cGMP, among others are presented in prostates from both rodents and human 3 . Substances that augment the intracellular levels of cGMP such as the NO‐donors, the sGC stimulators (BAY 41‐2272, BAY 63‐2521, vericiguat) or activators (BAY 60‐2770, BAY 58‐2667) and the PDE5 inhibitors promote prostate smooth muscle relaxation, 16 improve prostate blood supply 17 and reduce prostate smooth muscle and epithelial cells proliferation 18–20 …”

“…3 Substances that augment the intracellular levels of cGMP such as the NO-donors, the sGC stimulators (BAY 41-2272, BAY 63-2521, vericiguat) or activators (BAY 60-2770, BAY 58-2667) and the PDE5 inhibitors promote prostate smooth muscle relaxation, 16 improve prostate blood supply 17 and reduce prostate smooth muscle and epithelial cells proliferation. [18][19][20] In middle-age (10 months-old) rats, the prostate weight was greater and the expression of sGC subunits and the relaxation induced by NO were significantly reduced in comparison with prostate from young rats (3 month-old). 21 Older mice (>24 months) presented prostate nodules and a functional characteristics of BPH/bladder outlet obstruction as evidenced by delayed voiding response and elevated intravesical pressure in comparison with adult mice (2-12 months).…”

Comparative RNA-sequencing analysis of the prostate in a mouse model of benign prostatic hyperplasia with bladder outlet obstruction

“…Antioxidant stress may become a new therapeutic target for BPH; for example, previous studies have found that the lipid extract from the fruit of the Royal Palm of Cuba may treat prostatic hyperplasia through antioxidation [ 67 ]. GO terms enriched in the downregulated DEGs were associated with ion transport [ 68 ], whereas the upregulated DEGs were enriched in hormonal regulation, and previous studies had demonstrated the involvement of both androgens and oestrogens in the progression of BPH[ 23 , 69 ]. In addition, the results of KEGG analysis suggested that the most significant pathway was small molecules, which had been shown in previous studies to influence the cell cycle, apoptosis and proliferation [ 70 – 72 ], whereas the upregulated DEGs were most significantly enriched in pathways associated with IGFs and IGFBPs, which have been previously shown to be associated with BPH [ 28 , 73 ], and inhibition of IGF-1 secretion inhibited the proliferation of prostate epithelial cells [ 29 ].…”