scholarly journals Intracellular Ca2+-Mediated AE2 Is Involved in the Vectorial Movement of HaCaT Keratinocyte

2020 ◽  
Vol 21 (22) ◽  
pp. 8429
Author(s):  
Soyoung Hwang ◽  
Dong Min Shin ◽  
Jeong Hee Hong
Keyword(s):  
Wound Healing ◽  
Anion Exchanger ◽  
Skin Barrier ◽  
Chelating Agent ◽  
Hacat Keratinocytes ◽  
Keratinocyte Migration ◽  
Enhanced Expression ◽  
Hacat Keratinocyte ◽  
Stimulation Of ◽  
Exchange Activity

Keratinocyte migration is initiated toward the wound skin barrier as a crucial process in wound healing. However, the migratory machinery used by keratinocytes is relatively unknown. Histamine signaling, including an increase in the Ca2+ signal, mediated the enhanced protein expression and chloride/bicarbonate exchange activity of anion exchanger AE2 in keratinocytes. In this study, we applied an agarose spot assay to induce a vectorial motion. The vectorial stimulation of the histamine-containing agarose spot enhanced the HaCaT keratinocyte migration, compared to non-directional stimulation. AE2 is associated with the vectorial movement of HaCaT keratinocytes. Enhanced expression of AE2 was mainly associated with an increase in Ca2+ and was abolished by the treatment with the Ca2+ chelating agent BAPTA-AM. These findings revealed that the directionality of Ca2+-exerted stimulation can play a prominent role in facilitating migration through the involvement of AE2 as a migratory machinery in HaCaT keratinocytes.

scholarly journals FOXO1 differentially regulates both normal and diabetic wound healing

2015 ◽  
Vol 209 (2) ◽  
pp. 289-303 ◽  
Author(s):  
Chenying Zhang ◽  
Bhaskar Ponugoti ◽  
Chen Tian ◽  
Fanxing Xu ◽  
Rohinton Tarapore ◽  
...  
Keyword(s):  
Wound Healing ◽  
High Glucose ◽  
Dependent Manner ◽  
Downstream Targets ◽  
Keratinocyte Migration ◽  
Normal Wound Healing ◽  
Normal Glucose ◽  
Enhanced Expression ◽  
Diabetic Wounds ◽  
The Impact

Healing is delayed in diabetic wounds. We previously demonstrated that lineage-specific Foxo1 deletion in keratinocytes interfered with normal wound healing and keratinocyte migration. Surprisingly, the same deletion of Foxo1 in diabetic wounds had the opposite effect, significantly improving the healing response. In normal glucose media, forkhead box O1 (FOXO1) enhanced keratinocyte migration through up-regulating TGFβ1. In high glucose, FOXO1 nuclear localization was induced but FOXO1 did not bind to the TGFβ1 promoter or stimulate TGFβ1 transcription. Instead, in high glucose, FOXO1 enhanced expression of serpin peptidase inhibitor, clade B (ovalbumin), member 2 (SERPINB2), and chemokine (C-C motif) ligand 20 (CCL20). The impact of high glucose on keratinocyte migration was rescued by silencing FOXO1, by reducing SERPINB2 or CCL20, or by insulin treatment. In addition, an advanced glycation end product and tumor necrosis factor had a similar regulatory effect on FOXO1 and its downstream targets and inhibited keratinocyte migration in a FOXO1-dependent manner. Thus, FOXO1 expression can positively or negatively modulate keratinocyte migration and wound healing by its differential effect on downstream targets modulated by factors present in diabetic healing.

scholarly journals Ginsenosides repair UVB-induced skin barrier damage in BALB/c hairless mice and HaCaT keratinocytes

2021 ◽  
Author(s):  
Zhenzhuo Li ◽  
Rui Jiang ◽  
Manying Wang ◽  
Lu Zhai ◽  
Jianzeng Liu ◽  
...  
Keyword(s):  
Skin Barrier ◽  
Hacat Keratinocytes ◽  
Hairless Mice

Leucine-rich glioma inactivated 3 promotes HaCaT keratinocyte migration

2013 ◽  
Vol 21 (4) ◽  
pp. 634-640 ◽  
Author(s):  
Yun-Mi Jeong ◽  
Woo-Jae Park ◽  
Myo-Kyoung Kim ◽  
Kwang Jin Baek ◽  
Nyoun Soo Kwon ◽  
...  
Keyword(s):  
Keratinocyte Migration ◽  
Hacat Keratinocyte

Recent perspectives of nanotechnology in burn wounds management: a review

2021 ◽  
Vol 30 (5) ◽  
pp. 350-370
Author(s):  
Ruan Na ◽  
Tian Wei
Keyword(s):  
Wound Healing ◽  
Wound Closure ◽  
Healing Process ◽  
Skin Barrier ◽  
Active Role ◽  
Qualitative Studies ◽  
Future Directions ◽  
Burn Wounds ◽  
The Us ◽  
Efficacious Drug

Objective: The burden of the management of problematic skin wounds characterised by a compromised skin barrier is growing rapidly. Almost six million patients are affected in the US alone, with an estimated market of $25 billion annually. There is an urgent requirement for efficient mechanism-based treatments and more efficacious drug delivery systems. Novel strategies are needed for faster healing by reducing infection, moisturising the wound, stimulating the healing mechanisms, speeding up wound closure and reducing scar formation. Methods: A systematic review of qualitative studies was conducted on the recent perspectives of nanotechnology in burn wounds management. Pubmed, Scopus, EMBASE, CINAHL and PsychINFO databases were all systematically searched. Authors independently rated the reporting of the qualitative studies included. A comprehensive literature search was conducted covering various resources up to 2018–2019. Traditional techniques aim to simply cover the wound without playing any active role in wound healing. However, nanotechnology-based solutions are being used to create multipurpose biomaterials, not only for regeneration and repair, but also for on-demand delivery of specific molecules. The chronic nature and associated complications of nonhealing wounds have led to the emergence of nanotechnology-based therapies that aim at facilitating the healing process and ultimately repairing the injured tissue. Conclusion: Nanotechnology-based therapy is in the forefront of next-generation therapy that is able to advance wound healing of hard-to-heal wounds. In this review, we will highlight the developed nanotechnology-based therapeutic agents and assess the viability and efficacy of each treatment. Herein we will explore the unmet needs and future directions of current technologies, while discussing promising strategies that can advance the wound-healing field

scholarly journals EGF hijacks miR-198/FSTL1 wound-healing switch and steers a two-pronged pathway toward metastasis

2017 ◽  
Vol 214 (10) ◽  
pp. 2889-2900 ◽  
Author(s):  
Gopinath M. Sundaram ◽  
Hisyam M. Ismail ◽  
Mohsin Bashir ◽  
Manish Muhuri ◽  
Candida Vaz ◽  
...  
Keyword(s):  
Wound Healing ◽  
Wound Closure ◽  
Prognostic Significance ◽  
Competitive Inhibitor ◽  
Molecular Switch ◽  
Extracellular Signal Regulated Kinase ◽  
Keratinocyte Migration ◽  
Extracellular Signal ◽  
Single Transcript ◽  
Kinase Phosphorylation

Epithelial carcinomas are well known to activate a prolonged wound-healing program that promotes malignant transformation. Wound closure requires the activation of keratinocyte migration via a dual-state molecular switch. This switch involves production of either the anti-migratory microRNA miR-198 or the pro-migratory follistatin-like 1 (FSTL1) protein from a single transcript; miR-198 expression in healthy skin is down-regulated in favor of FSTL1 upon wounding, which enhances keratinocyte migration and promotes re-epithelialization. Here, we reveal a defective molecular switch in head and neck squamous cell carcinoma (HNSCC). This defect shuts off miR-198 expression in favor of sustained FSTL1 translation, driving metastasis through dual parallel pathways involving DIAPH1 and FSTL1. DIAPH1, a miR-198 target, enhances directional migration through sequestration of Arpin, a competitive inhibitor of Arp2/3 complex. FSTL1 blocks Wnt7a-mediated repression of extracellular signal–regulated kinase phosphorylation, enabling production of MMP9, which degrades the extracellular matrix and facilitates metastasis. The prognostic significance of the FSTL1-DIAPH1 gene pair makes it an attractive target for therapeutic intervention.

scholarly journals Acceleration of Sodium-Calcium Exchange Activity during ATP-induced Calcium Release in Transfected Chinese Hamster Ovary Cells

1997 ◽  
Vol 109 (1) ◽  
pp. 53-60 ◽  
Author(s):  
Melissa Vázquez ◽  
Yu Fang ◽  
John P. Reeves
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Chinese Hamster Ovary ◽  
Calcium Release ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Ovary Cells ◽  
Kinase C ◽  
Stimulation Of ◽  
Exchange Activity

The P2U purinergic agonist ATP (0.3 mM) elicited an increase in [Ca2+]i due to Ca2+ release from intracellular stores in transfected Chinese hamster ovary cells that express the bovine cardiac Na+/Ca2+ exchanger (CK1.4 cells). The following observations indicate that ATP-evoked Ca2+ release was accompanied by a Ca2+- dependent regulatory activation of Na+/Ca2+ exchange activity: Addition of extracellular Ca2+ (0.7 mM) 0–1 min after ATP evoked a dramatic rise in [Ca2+]i in Na+-free media (Li+ substitution) compared to Na+-containing media; no differences between Na+- and Li+-based media were observed with vector-transfected cells. In the presence of physiological concentrations of extracellular Na+ and Ca2+, the ATP-evoked rise in [Ca2+]i declined more rapidly in CK1.4 cells compared to control cells, but then attained a long-lived plateau of elevated [Ca2+]i which eventually came to exceed the declining [Ca2+]i values in control cells. ATP elicited a transient acceleration of exchange-mediated Ba2+ influx, consistent with regulatory activation of the Na+/Ca2+ exchanger. The acceleration of Ba2+ influx was not observed in vector-transfected control cells, or in CK1.4 cells in the absence of intracellular Na+ or when the Ca2+ content of the intracellular stores had been reduced by prior treatment with ionomycin. The protein kinase C activator phorbol 12-myristate 13-acetate attenuated the exchange-mediated rise in [Ca2+]i under Na+-free conditions, but did not inhibit the ATP-evoked stimulation of Ba2+ influx. The effects of PMA are therefore not due to inhibition of exchange activity, but probably reflect the influence of protein kinase C on other Ca2+ homeostatic mechanisms. We conclude that exchange activity is accelerated during ATP-evoked Ca2+ release from intracellular stores through regulatory activation by increased [Ca2+]i. In the absence of extracellular Ca2+, the stimulation of exchange activity is short-lived and follows the time course of the [Ca2+]i transient; in the presence of extracellular Ca2+, we suggest that the exchanger remains activated for a longer period of time, thereby stabilizing and prolonging the plateau phase of store-dependent Ca2+ entry.

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