CBAC Seminar Series - W Jonathan Lederer, MD, PhD - Shared screen with speaker view
huyen nguyen
Good morning/afternoon everyone from around the world! Welcome to the CBAC Seminar Series! Please remember the following during the presentation:1) To turn on the Speaker Spotlight: Go to the top right corner, click the three vertical dots, and select “Spotlight Speaker.”2) If you have any questions, please post your message to everyone. 3) Remember to keep yourself muted throughout the presentation.
huyen nguyen
If you have any questions, please post your message to everyone.
Guy Salama
What is the APD level in these graphs of ATP vs. voltage? Is it not running out and rate limiting?
Coert Zuurbier
Beautiful and clear talk. Have you ever been able to look when you increase extracellular Na the mito Ca or ATP production goes down?
Mohamed Trebak
Outstanding talk Jon! 1) in non-excitable cells, cytosolic Ca2+ oscillations are mirrored by rapid oscillations in mitochondrial ca2+. Why do you think MCU in CM is different? 2) Related to 1) Vamsi Mootha measured the Kd of MICU1/2 dimers to Ca2+=650nM. Based on MCU uptake in CM you showed, do you think CM have no MICU gatekeeping?3) Do you think the ca2+-dependent activation of alphaKGD and SDH is not real or just not found in CM?
Guy Salama
Does pyruvate cross the cell membrane? and how?
Douglas Mann
Do your findings explain why inotropes that increase Ca++ influx lead to problems with cardiac injury
Barry London
Wonderful work! Have you looked to see if mitochondria from heart failure models behave differently?
David Eisner
Jon - when you increased rate with a "Ca-independent " fuel the mitochondria depolarized. However, the potential did not seem to recover when you returned to slow rate. What's happening?
sandor kovacs
given that mammalian heart rates range from 600 or more beats per minute to a few beats per minute -whast differences do you expect in the expect mitochondria of a mouse vs a blue whale to be
David Eisner
Re Mohamed Trebak question. One difference between heart and non excitable cells is that the rises of ca in heart are so brief that there isn't time for matrix Ca to follow it
Mohamed Trebak
Thanks very much David!
Druv Bhagavan
Awesome talk! You discussed matrix Ca as essentially following intracellular Ca (and thus serving to regulate ATP production). Does the reverse occur? I.e. does matrix Ca have a significant impact on intracellular Ca?
Sarah M. Schumacher
Do you think a combination of these Ca dependent and independent pathways would be more efficient for a stressed heart, vs metabolic switch?
Druv Bhagavan
Thank you, that was what I was getting at!
Abigail Bartlett
Great talk thanks!
Colin Nichols
fascinating- thanks Jon!
Kamila Bledzka
thank you