Can someone also start a discussion trend for this plzzzz
Anyone get that question that said what would happen to frataxin production in mice with fff, all lowercase? Did you say an increase or decrease would occur because I’m still lost.
So I designed a few species of
I want to know how best to design a species to be able to compete with them
Mitochondria are fascinating structures of the cellular compartments that generate energy to run the cells. However, inherent disorders of mitochondria due to diabetes can cause major disruption of metabolism that produces huge amount of reactive oxygen species (ROS). Here we study the elevated level of ROS provoked by high glucose (HG) environment triggered mitochondrial dysfunction, inflammatory response and apoptosis via stress signalling pathway in keratinocytes. Our results demonstrated that elevated glucose level in keratinoctes, increase the accumulations of ROS and decrease in cellular antioxidant capacities. Moreover, excess production of ROS was associated with mitochondrial dysfunction, characterized by loss of mitochondrial membrane potential (ΔΨm), increase in mitochondrial mass, alteration of mitochondrial respiratory complexes, cytochrome c (Cyt c) release, decrease in mitochondrial transcription factor A (TFAM) and increase in mitochondrial DNA (mtDNA) fragmentation. Damaged mtDNA escaped into the cytosol, where it engaged the activation of ERK1/2, PI3K/Akt, tuberin and mTOR via cGAS-STING leading to IRF3 activation. Pre-treatment of pharmacological inhibitors, ERK1/2 or PI3K/Akt suppressed the IRF3 activation. Furthermore, our results demonstrated that activation of IRF3 in HG environment coinciding with increased expression of inflammatory mediators. Excess production of ROS interfered with decreased in cell viability, increased lysosomal content and expression of FoxOs, leading to cell cycle deregulation and apoptosis. Pre-treatment of N-acetyl-l-cysteine (NAC) significantly reduced the HG-induced cell cycle deregulation and apoptosis in keratinocytes. In conclusion, increased oxidative stress underlies the decrease in antioxidant capacities and mitochondrial dysfunction in HG environment correlate with inflammation response and apoptosis via ERK1/2-PI3K/Akt-IRF3 p... keep reading on reddit ➡
Hi, I recently started teaching myself biology because I'm doing it in my first year of university (next year), and I've never taken it before (applied math/physics major), so I'm sorry if this is a dumb/easy question.
Where is the keratin in keratinocytes? Do keratinocytes secrete keratin? Is keratin highly concentrated in their membrane (like an integral protein)? Does the keratin provide internal support like a cytoskeleton? Or does keratin help make up the ground substance of the extracellular matrix around them?
Please let me know if I've got any major conceptual flaws here, haha.
In vitro research, investigating the protective potential of proteo-glycans (aka PSP, a beta-glucan linked to a peptide, which are said to be the main bioactive ingredients in Turkey Tail) . Quite technical.
The conclusion was that PSP, a natural antioxidant, may be effective for attenuating free radical‐induced oxidative damage in human skin.
Full paper is here.
Also see this related research.
So our lab will be receiving some patient skin tissues soon that I will need to establish, subculture, and cyro for future work. Since I only have experience with pre-established cultures of primary keratinocytes I had a few questions I was hoping someone could answer. My PI is not a biologist (medicinal chemist) and none of my committee members have established primary keratinocytes from tissue before. These are rare and precious samples so I cannot afford to lose them with mistakes, I was actually thinking of practicing a few times on some of my skin (maybe just a few hair follicles) just so I know it will work before I handle the patient tissues.
I am using this protocol as a general guide to the process.
-The protocol calls for use of coating matrix in the flasks seeded with the keratinocytes, however I have never used coating matrix in the past as we use t75 flasks that already allow for cell adhesion (for pre-established keratinocyte culture). Is this step only for labs using flasks that do not facilitate adhesion without addition of the matrix or is there another reason to use this in this situation even if we have adhesive flasks?
-If we also want to collect and sulture the fibroblasts from this same tissue the protocol recommends following this guide, however that protocol specifically calls for neonatal tissue and we will be using adult tissue. Is there any reason I cannot follow this protocol for adult tissue? What differences are there when isolating adult fibroblasts rather than neonatal? The protocol mentions for adult tissue to use more tissue and increase collagenase but how much should I increase this by?
-Recombinant Trypsin/EDTA vs "regular" TE? What is the difference and should it matter? Can I just use the TE I have used in the past?keep reading on reddit ➡
Cannabinoids inhibit human keratinocyte proliferation through a non-CB1/CB2 mechanism and have a potential therapeutic value in the treatment of psoriasis.
AuthorsWilkinson JD, et al. Show all Journal J Dermatol Sci. 2007 Feb;45(2):87-92. Epub 2006 Dec 6.