So I was wondering and it's pretty interesting Lauster et al talks about this.;
I understand the reference to cell growth as minoxidil has shown to influence pathways like ERK/AKT, BCL-2/BAX etc.
However the reference to senescence is particularly interesting. I haven't seen really seen minoxidil directly mentioned to influence senescence in any study that I know of. Is there a study I'm not aware of maybe which talks about minoxidil and senescence in a direct way? Anyone know?
@InBeforeTheCure?
Or does he mean the studies that show minoxidil can affect pathways like P16ink4a, P21 etc. that can be/are implicated in senescence?
Hi
I found 2 studies but I don't know if these studies are helping...
1. One of them called "
The investigation of minoxidil-induced [Ca2+]i rises and non-Ca2+-triggered cell death in PC3 human prostate cancer cells. " 2016 Jun
Abstract
Minoxidil is clinically used to prevent hair loss. However, its effect on Ca2+ homeostasis in prostate cancer cells is unclear. This study explored the effect of minoxidil on cytosolic-free Ca2+ levels ([Ca2+]i) and cell viability in PC3 human prostate cancer cells. Minoxidil at concentrations between 200 and 800 μM evoked [Ca2+]i rises in a concentration-dependent manner. This Ca2+ signal was inhibited by 60% by removal of extracellular Ca2+. Minoxidil-induced Ca2+ influx was confirmed by Mn2+-induced quench of fura-2 fluorescence. Pre-treatment with the protein kinase C (PKC) inhibitor GF109203X, PKC activator phorbol 12-myristate 13 acetate (PMA), nifedipine and SKF96365 inhibited minoxidil-induced Ca2+ signal in Ca2+ containing medium by 60%. Treatment with the endoplasmic reticulum Ca2+ pump inhibitor 2,5-ditert-butylhydroquinone (BHQ) in Ca2+-free medium abolished minoxidil-induced [Ca2+]i rises. Conversely, treatment with minoxidil abolished BHQ-induced [Ca2+]i rises. Inhibition of phospholipase C (PLC) with U73122 abolished minoxidil-evoked [Ca2+]i rises.
Overnight treatment with minoxidil killed cells at concentrations of 200-600 μM in a concentration-dependent fashion. Chelation of cytosolic Ca2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/AM (BAPTA/AM) did not prevent minoxidil's cytotoxicity. Together, in PC3 cells, minoxidil induced [Ca2+]i rises that involved Ca2+ entry through PKC-regulated store-operated Ca2+ channels and PLC-dependent Ca2+ release from the endoplasmic reticulum. Minoxidil-induced cytotoxicity in a Ca2+-independent manner.
2.
Arctiin blocks hydrogen peroxide-induced senescence and cell death though microRNA expression changes in human dermal papilla cells 2014
"In the present study, we found that arctiin exerts anti-oxidative effects on human hair dermal papilla cells (HHDPCs).
Results
To better understand the mechanism, we analyzed the level of hydrogen peroxide (H2O2)-induced cytotoxicity, cell death, ROS production and senescence after arctiin pretreatment of HHDPCs"
" Also, TAK1/MAP3K7 deficiency upregulates ROS levels, resulting in skin keratinocyte cell death [
34]. Extracellular signal-regulated kinase (
ERK), a member of the MAPK family, plays an important role in HHDPC proliferation.
ERK signaling is activated by minoxidil, which is a widely used drug for treating androgenetic alopecia, and ERK inhibition blocks the anti-alopecia effect of the minoxidil [
35]. In addition, our bioinformatic results showed that MAPK signaling was the most commonly targeted pathway for the downregulated miRNAs mediated by arctiin in HHDPCs (Table
5). This result indicates that MAPK pathway activation is important for HHDPC proliferation. However, our bioinformatic analysis revealed that the MAPK signaling pathway is also targeted by the upregulated miRNAs (Table
4), indicating that inhibition of MAPK signaling pathway might be involved in protective effects against ROS in HHDPCs. It has been reported that ROS activates ERK/MAPK, and
ROS-mediated ERK activation induces apoptosis and senescence in several cell lines"
