Real-time polymerase chain reaction (PCR) results showed that two chemokines (CXCL10, CXCL12) were highly expressed during the formation of normal scar, and there was almost no expression during the formation of hypertrophic scar (*P < 0.05).
Lastly, using hypertrophic scar-derived fibroblasts, we showed that the elevated α-SMA and collagen I levels were markedly reduced after treatment with Wnt4.
The chemokines (CCL2, CCL3, CCL4, CCL5, CCL7, CCL13, CX3CL1) were almost non-expressed in the formation of normal scars but were expressed for a long time in the formation of hypertrophic scars.
To investigate the efficacy of cell penetrating peptide TAT-modified liposomes loaded with salvianolic acid B (SAB-TAT-LIP) on the proliferation, migration, survival, and TGF-β<sub>1</sub> expression of human skin fibroblasts (HSF) and to preliminarily evaluate its effect on the prevention and treatment of hypertrophic scars.
SIP1 expression was markedly lower in HS vs. normal skin (NS) tissue, and α-smooth muscle actin (α-SMA) content and collagen I/III (Col I/III) synthesis were inversely correlated with SIP1 expression.
Moreover, the hypertrophic scar fibroblast (HSF) cells were isolated from HS tissues and divided into four groups according to different treatment methods: blank control group, scramble-transfected negative control group, miR-564 inhibitor-transfected miR-564 inhibitor group, and miR-564 plasmid-transfected miR-564 mimic group.
Immoderate proliferation and deposition of collagen generally result in hypertrophic scars and even keloids. microRNA-29 (miR-29) has been proved as a crucial regulator in these pathological processes.
SIP1 expression was markedly lower in HS vs. normal skin (NS) tissue, and α-smooth muscle actin (α-SMA) content and collagen I/III (Col I/III) synthesis were inversely correlated with SIP1 expression.
SIP1 expression was markedly lower in HS vs. normal skin (NS) tissue, and α-smooth muscle actin (α-SMA) content and collagen I/III (Col I/III) synthesis were inversely correlated with SIP1 expression.
Increased expression of DDR1 has been documented in several types of cancer and fibrotic conditions including skin hypertrophic scars, idiopathic pulmonary fibrosis, cirrhotic liver and renal fibrosis.
Our findings show that miR-495 inhibits FAK and its downstream mediators in vitro and vivo, and suggest that miR-495 may be a useful therapeutic target for the treatment of hypertrophic scar.
The function of miR-205-5p on cell proliferation was detected using Cell Counting Kit-8 assay, and cell apoptosis was detected via flow cytometry. miR-205-5p expression was decreased in HS tissues and human hypertrophic scar fibroblasts (hHSFs).
Propranolol, a nonspecific β1-, β2-adrenergic receptor (AR) inverse agonist, counters the hypermetabolic response to elevated catecholamines and may decrease hypertrophic scarring by an unknown mechanism.
The expression of TSP-4 was compared on both mRNA and protein levels between hypertrophic scar fibroblasts (HSFs) and normal skin fibroblast (NFs) in response to TGF-β1 treatment.