I am thrilled to release our latest preprint from @AmiLang_Science, out today @biorxivpreprint! Local erythropoiesis directs oxygen availability in bone fracture repair https://t.co/U97vXTwOS6 A paper thread:

Our problem is not that our society does not sufficiently appreciate the economic return on investment in science. It is that we value education and knowledge generation only in economic terms.

it is my distinguished honor to be this year's Spring Commencement Speaker at @PittBradford! https://t.co/L8JvB9kCM1

An public service announcement: Sinclair Lewis’s “It Can’t Happen Here” is in the public domain. https://t.co/Qjz2LmCEmL

Huge congrats Dr. @StphanePetrousk!! And many thanks @HoeyLab for the fantastic visit!

Tomorrow is @madhura0327’s Ph.D. thesis defense! I’m so proud of everything she’s accomplished. If at Penn, hope you can make it. If you’d like a zoom link, just reach out to Madhura. “The Role of YAP in Bone Fracture Repair” 3.00 PM, Reunion Auditorium John Morgan Building

Returning home rejuvenated by time w so many dear friends at #ORS2025 Also so proud and thankful for my group. Special congrats to @cpane94 on winning the NIRA, @AmiLang_Science on @isfrfractures🥇Podium Award and @ESeidlScience on @ors_tendon 3MT Award 🙌

Wonder how maternal movements impact fetal skeletal development? Join my #ORS2025 NIRA talk! @isfrfractures @orssociety @jboerckel #OrthoTwitter 🗓️TODAY (2/9) at 11:47 AM 📍 West 301BC

Excited for #ORS2025 and super proud of this group who will be presenting their work! 🙌🏻 @Madhura0327 @GeorgeKotsaris @ESeidlScience @AmiLang_Science @cpane94 ht @cpane94 for the slide!

Excited to debut my vision for the Panebianco Lab™️ at #ORS2025 ! @ORSsociety #OrthoTwitter #FuturePI

So proud of our latest work 😍🦴🩸 This project was a rollercoaster 🎢, but I loved every moment of it. Huge thanks to all amazing collaboration partners at UPenn 👩‍🔬🧑‍💻👨‍🔬🧑‍💼 Don’t miss the perfect thread by @jboerckel breaking it all down 👇Funded by #MSCA #Postdoc

So wonderful to have @JoyYWu as @Penn_PCMD Visting Professor! Thanks for the great talk, Joy!

So, next time you’re doing algebra, I hope it reminds you of the remarkable process of bone fracture repair. This has been the most surprising and exhilarating ride. We would love feedback as we send this paper for peer review: https://t.co/Mhtjay1XIL

Together, these data upend our current understanding of the early phase of bone fracture repair, provide a mechanism for high oxygen tension in the bone marrow after injury, and reveal an unexpected and targetable role of erythroid progenitors in fracture repair.

Remarkably, making the fracture site hypoxic promoted angiogenesis and increased bone formation.

Annemarie then did a cool experiment: she treated fractures with a CD71-blocking antibody, which prevents iron import. CD71 blockade arrested heme synthesis and made the fracture site hypoxic!

These erythroid progenitor cells express CD71, or Transferrin receptor 1. Erythroid cells are super iron-hungry, as they begin to make hemoglobin, which uses iron to bind oxygen. Transferrin receptor is the primary iron transporter in these cells.

We found that fracture activated local erythroid progenitor cells, without a change in serum EPO!

Now, when a bone is fractured, it breaks the bone and ruptures the vessels, but it also breaks the bone marrow. Bone marrow is special because it is the site of erythropoiesis: the production of new red blood cells from stem cells.

What could cause this high oxygen? Fracture rapidly causes hematoma formation, which arrests bleeding and cuts off the supply of new erythrocytes. So, we took a single cell approach to identify the cell populations at the fracture site, compared to contralateral bone marrow.

We measured bone marrow at ~30mmHg as expected, but the oxygen at the early fracture site was almost 60 mmHg - higher in oxygen than the spleen, which is rich in oxygenated red blood cells.