Miguel Martín-Aragón Baudel

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  Miguel Martín-Aragón Baudel miguelmab.bsky.social · Jul 10, 2025
  Check our latest work from the M&M lab on the role of SMC Pannexin 1 in diabetic hyperglycemia! And thanks to everyone involved in this! Ole 💃 www.ahajournals.org/doi/10.1161/...
  

  Arterial Myocyte Pannexin 1 Channel Controls Vascular Reactivity in Diabetic Hyperglycemia | Circulation Research

  BACKGROUND: Diabetic hyperglycemia promotes vasoconstriction by activating an ATP-dependent P2Y11L (P2Y11-like receptor)/AC5 (adenylyl cyclase 5)/AKAP5 (A-kinase anchoring protein 5)/PKA (protein kina...

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  Miguel Martín-Aragón Baudel miguelmab.bsky.social · Jan 30, 2025
  A very nice surprise to find a fantastic editorial by @tomjhund of our recently published work at @CircRes which is now open access! ahajournals.org/doi/10.1161/CI…

  Spatiotemporal Control of Vascular CaV1.2 by α1C S1928 Phosphorylation | Circulation Research

  Background: L-type CaV1.2 channels undergo cooperative gating to regulate cell function, although mechanisms are unclear. This study tests the hypothesis that phosphorylation of the CaV1.2 pore-forming subunit α1C at S1928 mediates vascular CaV1.2 cooperativity during diabetic hyperglycemia. Methods: A multiscale approach including patch-clamp electrophysiology, super-resolution nanoscopy, proximity ligation assay, calcium imaging‚ pressure myography, and Laser Speckle imaging was implemented to examine CaV1.2 cooperativity, α1C clustering, myogenic tone, and blood flow in human and mouse arterial myocytes/vessels. Results: CaV1.2 activity and cooperative gating increase in arterial myocytes from patients with type 2 diabetes and type 1 diabetic mice, and in wild-type mouse arterial myocytes after elevating extracellular glucose. These changes were prevented in wild-type cells pre-exposed to a PKA inhibitor or cells from knock-in S1928A but not S1700A mice. In addition, α1C clustering at the surface membrane of wild-type, but not wild-type cells pre-exposed to PKA or P2Y11 inhibitors and S1928A arterial myocytes, was elevated upon hyperglycemia and diabetes. CaV1.2 spatial and gating remodeling correlated with enhanced arterial myocyte Ca2+ influx and contractility and in vivo reduction in arterial diameter and blood flow upon hyperglycemia and diabetes in wild-type but not S1928A cells/mice. Conclusions: These results suggest that PKA-dependent S1928 phosphorylation promotes the spatial reorganization of vascular α1C into “superclusters” upon hyperglycemia and diabetes. This triggers CaV1.2 activity and cooperativity, directly impacting vascular reactivity. The results may lay the foundation for developing therapeutics to correct CaV1.2 and arterial function during diabetic hyperglycemia. Graphical Abstract

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  Miguel Martín-Aragón Baudel miguelmab.bsky.social · Jan 30, 2025
  Finally out! Big thanks to all the team for making this important piece of work possible! @mf_navedo @MNCline @VicTamez88 @Rebound_32 @raghureddy92 @_abbyburns and collaborators. Olé💃🏻 Spatiotemporal Control of Vascular CaV1.2 by α1C S1928 Phosphorylation ahajournals.org/doi/abs/10.116…

  Spatiotemporal Control of Vascular CaV1.2 by α1C S1928 Phosphorylation | Circulation Research

  Background: L-type CaV1.2 channels undergo cooperative gating to regulate cell function, although mechanisms are unclear. This study tests the hypothesis that phosphorylation of the CaV1.2 pore-forming subunit α1C at S1928 mediates vascular CaV1.2 cooperativity during diabetic hyperglycemia. Methods: A multiscale approach including patch-clamp electrophysiology, super-resolution nanoscopy, proximity ligation assay, calcium imaging‚ pressure myography, and Laser Speckle imaging was implemented to examine CaV1.2 cooperativity, α1C clustering, myogenic tone, and blood flow in human and mouse arterial myocytes/vessels. Results: CaV1.2 activity and cooperative gating increase in arterial myocytes from patients with type 2 diabetes and type 1 diabetic mice, and in wild-type mouse arterial myocytes after elevating extracellular glucose. These changes were prevented in wild-type cells pre-exposed to a PKA inhibitor or cells from knock-in S1928A but not S1700A mice. In addition, α1C clustering at the surface membrane of wild-type, but not wild-type cells pre-exposed to PKA or P2Y11 inhibitors and S1928A arterial myocytes, was elevated upon hyperglycemia and diabetes. CaV1.2 spatial and gating remodeling correlated with enhanced arterial myocyte Ca2+ influx and contractility and in vivo reduction in arterial diameter and blood flow upon hyperglycemia and diabetes in wild-type but not S1928A cells/mice. Conclusions: These results suggest that PKA-dependent S1928 phosphorylation promotes the spatial reorganization of vascular α1C into “superclusters” upon hyperglycemia and diabetes. This triggers CaV1.2 activity and cooperativity, directly impacting vascular reactivity. The results may lay the foundation for developing therapeutics to correct CaV1.2 and arterial function during diabetic hyperglycemia. Graphical Abstract

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  Miguel Martín-Aragón Baudel miguelmab.bsky.social · Jan 30, 2025
  A new exciting review article form our lab together with @eric_psilva @MNCline and @mf_navedo. And more in the oven!  🔥 Ion channel molecular complexes in vascular smooth muscle frontiersin.org/articles/10.33…

  Frontiers | Ion channel molecular complexes in vascular smooth muscle

  Ion channels that influence membrane potential and intracellular calcium concentration control vascular smooth muscle excitability. Voltage-gated calcium cha...

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  Miguel Martín-Aragón Baudel miguelmab.bsky.social · Jan 30, 2025
  Come to sunny California and join us, so many cool projects going on! x.com/mf_navedo/stat…
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  Miguel Martín-Aragón Baudel miguelmab.bsky.social · Jan 30, 2025
  If you're looking for a postdoc in a top lab, with top tools and a top mentor, come to Davis! x.com/MNCline/status…
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  Miguel Martín-Aragón Baudel miguelmab.bsky.social · Jan 30, 2025
  Pretty chuffed about getting my AHA Postdoctoral Fellowship!! Thanks to @AHA_Research and obviously @mf_navedo and @MNCline. Olé 💃
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  Miguel Martín-Aragón Baudel miguelmab.bsky.social · Jan 30, 2025
  Excited to announce that we will be presenting our work examining the role of TRPC channels in store-operated-Ca2+ entry in the vasculature in the Virtual Journal Club by @ThePhySoc 16 September 15:00 -15:45 BST FREE Registration: bit.ly/2EN8B7Q

  Role of PKC / TRPC1 Channels in PIP2 Mediated Store Operated Ca2+ Influx in Vascular Smooth Muscle

  Find info about The Physiological Society's events, including scientific conferences, exhibition, sponsorship, first meeting advice, abstracts, and themes.

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