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Cell-penetrating peptides, targeting the regulation of store-operated channels, slow decay of the progesterone-induced [Ca2+]i signal in human sperm.

Morris J, Jones S, Howl J, Lukanowska M, Lefievre L, Publicover S - Mol. Hum. Reprod. (2015)

Bottom Line: Resting [Ca(2+)]i temporarily decreased upon application of KIKKK peptide (3-4 min), but scrambled KIKKK peptide had a similar effect, indicating that this action was not sequence-specific.Examination of single-cell responses showed that this effect was due, at least in part, to an increase in the proportion of cells in which the initial transient was maintained for an extended period, lasting up to 10 min in a subpopulation of cells.We hypothesize that SOCs contribute to the progesterone-induced [Ca(2+)]i transient, and that interference with the regulatory mechanisms of SOC delays their closure, causing a prolongation of the [Ca(2+)]i transient.

View Article: PubMed Central - PubMed

Affiliation: School of Biosciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.

No MeSH data available.


Related in: MedlinePlus

Prolonged [Ca2+]i responses in human sperm are not due to mitochondrial Ca2+ accumulation. (a) Montage shows a pseudocolour image series of a 5-µM KIKKK-pretreated cell which shows a prolonged [Ca2+]i response. Images are at 1 min intervals (indicated by adjacent numbers). Progesterone was added just before image 9. Note that increased [Ca2+]i at the posterior head/neck (PHN) is maintained for >4 min. (b) Four examples showing separate analysis of [Ca2+]i responses in the midpiece (green) and PHN region (blue) in the same cell. KIKKK was added at the arrow; yellow bars show application of 3 µM progesterone. Responses occur simultaneously the PHN and midpiece.
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GAV019F4: Prolonged [Ca2+]i responses in human sperm are not due to mitochondrial Ca2+ accumulation. (a) Montage shows a pseudocolour image series of a 5-µM KIKKK-pretreated cell which shows a prolonged [Ca2+]i response. Images are at 1 min intervals (indicated by adjacent numbers). Progesterone was added just before image 9. Note that increased [Ca2+]i at the posterior head/neck (PHN) is maintained for >4 min. (b) Four examples showing separate analysis of [Ca2+]i responses in the midpiece (green) and PHN region (blue) in the same cell. KIKKK was added at the arrow; yellow bars show application of 3 µM progesterone. Responses occur simultaneously the PHN and midpiece.

Mentions: In our previous work on the effects of 2-APB on the progesterone-induced [Ca2+]i signal, we observed strong enhancement of the sustained Ca2+ response that was localized specifically to the midpiece, possibly reflecting enhanced accumulation of Ca2+ in the mitochondria due to the effects of the drug on mitochondrial Ca2+ export (Lefievre et al., 2012). To assess whether the effect described here might be similar, we investigated the location of the [Ca2+]i signal. Prolonged responses occurred simultaneously in the midpiece and PHN of the sperm, showing that this effect was primarily on cytoplasmic [Ca2+]i and not due to Ca2+ accumulation within the mitochondrial matrix (Fig. 4).Figure 4


Cell-penetrating peptides, targeting the regulation of store-operated channels, slow decay of the progesterone-induced [Ca2+]i signal in human sperm.

Morris J, Jones S, Howl J, Lukanowska M, Lefievre L, Publicover S - Mol. Hum. Reprod. (2015)

Prolonged [Ca2+]i responses in human sperm are not due to mitochondrial Ca2+ accumulation. (a) Montage shows a pseudocolour image series of a 5-µM KIKKK-pretreated cell which shows a prolonged [Ca2+]i response. Images are at 1 min intervals (indicated by adjacent numbers). Progesterone was added just before image 9. Note that increased [Ca2+]i at the posterior head/neck (PHN) is maintained for >4 min. (b) Four examples showing separate analysis of [Ca2+]i responses in the midpiece (green) and PHN region (blue) in the same cell. KIKKK was added at the arrow; yellow bars show application of 3 µM progesterone. Responses occur simultaneously the PHN and midpiece.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4487447&req=5

GAV019F4: Prolonged [Ca2+]i responses in human sperm are not due to mitochondrial Ca2+ accumulation. (a) Montage shows a pseudocolour image series of a 5-µM KIKKK-pretreated cell which shows a prolonged [Ca2+]i response. Images are at 1 min intervals (indicated by adjacent numbers). Progesterone was added just before image 9. Note that increased [Ca2+]i at the posterior head/neck (PHN) is maintained for >4 min. (b) Four examples showing separate analysis of [Ca2+]i responses in the midpiece (green) and PHN region (blue) in the same cell. KIKKK was added at the arrow; yellow bars show application of 3 µM progesterone. Responses occur simultaneously the PHN and midpiece.
Mentions: In our previous work on the effects of 2-APB on the progesterone-induced [Ca2+]i signal, we observed strong enhancement of the sustained Ca2+ response that was localized specifically to the midpiece, possibly reflecting enhanced accumulation of Ca2+ in the mitochondria due to the effects of the drug on mitochondrial Ca2+ export (Lefievre et al., 2012). To assess whether the effect described here might be similar, we investigated the location of the [Ca2+]i signal. Prolonged responses occurred simultaneously in the midpiece and PHN of the sperm, showing that this effect was primarily on cytoplasmic [Ca2+]i and not due to Ca2+ accumulation within the mitochondrial matrix (Fig. 4).Figure 4

Bottom Line: Resting [Ca(2+)]i temporarily decreased upon application of KIKKK peptide (3-4 min), but scrambled KIKKK peptide had a similar effect, indicating that this action was not sequence-specific.Examination of single-cell responses showed that this effect was due, at least in part, to an increase in the proportion of cells in which the initial transient was maintained for an extended period, lasting up to 10 min in a subpopulation of cells.We hypothesize that SOCs contribute to the progesterone-induced [Ca(2+)]i transient, and that interference with the regulatory mechanisms of SOC delays their closure, causing a prolongation of the [Ca(2+)]i transient.

View Article: PubMed Central - PubMed

Affiliation: School of Biosciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.

No MeSH data available.


Related in: MedlinePlus