Meet the Erythrocyte

Meet the Erythrocyte

Red blood cells take up 45% of your blood volume and circulate about once in 20 seconds, carrying vital oxygen to every nook and cranny of your body. Did you know that ~2.4 million of these are produced each second? That’s because they have a short life span of only about 120 days.

Please squeeze me: The image shows a red blood cell squeezing through a tiny capillary: to accomplish this maneuver, the red cell sacrifices its nucleus and mitochondria to become a flexible, biconcave disk. In the inset, is a deformed red cell from a patient with sickle cell disease shown next to a normal cell. A single mutation in hemoglobin, the oxygen carrier of red blood cells, causes the proteins to clump giving the cells their characteristic sickle shape. The deformed cells block capillaries and burst more easily, surviving only 10-20 days. 

Heterozygote advantage: Given the severe health complications from sickle cell disease, why does the mutation persist in some populations? You might expect that negative selection against affected individuals would have eliminated the mutation. It turns out that carriers of the mutation (who have one normal copy and one mutated version of the gene), have mild sickling of their red blood cells which also makes them more resistant to infection by the malarial parasite. In fact, sickle cell disease is more common in areas where malaria is endemic. 

Another installment of an  #excyting  series on cells. This one is for Chad Haney who celebrates his birthday today and is my fellow conspirator in science outreach on Google Plus. Chad worked on generating a blood substitute as a graduate student. #HappyBirthdayChad   #HappyBirthdayMrMRI   #ScienceEveryday   #ScienceSunday  


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61 Responses to Meet the Erythrocyte

  1. Deeksha Tare says:

    It couldn’t be better Rajini Rao !

    Apt post for the man!!! 🙂

  2. Chad Haney says:

    Thanks Rajini Rao 

    Sifting through tons of notifications.

  3. Very much in keeping with both your styles and the spirit of the day — Kudos, Rajini Rao …

  4. That was the plan, Chad Haney …  heheheh

  5. Rajini Rao says:

    Hopefully a delightful task, Chad Haney ! Happy Birthday 🙂

  6. Chad Haney says:

    Thanks Remigiusz Raitza 

  7. Happy birthday Chad Haney  🙂

    And great post Rajini Rao .  I taught a course in bio/ genetic prenatal and infant development, and the students had a hard time understanding the concenpt of sickle cell anemia and why it persists as a trait.  I used to illustrate it with plush RBCs and tubes, but this is way cooler. 

  8. Pam Adger says:

    Happy Birthday Chad Haney!   

    Rajini Rao another great post. Thank you. 

  9. Rajini Rao says:

    Chryle Elieff , it’s an interesting genetic concept! There are other genetic diseases like it: phenylketouria, Tay-Sachs and possibly cystic fibrosis. Perhaps there is a good simulation program that randomly matches carriers and scores survival and persistence of the sickle cell allele with and without a heterozygous advantage..that would make a good teaching tool. 

  10. Rajini Rao says:

    So sorry to hear that, Roelf Renkema . What is the medical term of your condition? There must also be complications from iron toxicity in the liver?

  11. Chad Haney says:

    Thanks Chryle Elieff and Pam Adger 

    I should get the visualization guys at work to make a video about sickle cell vs. normal RBC. They did an awesome animation of action potentials from macro to nano scale. If it becomes public, I’ll either post it or link it to the lab webpage.

  12. Pam Adger says:

    Chad Haney That would be fantastic! 

  13. 夏子涵 says:

    It always looks like a donut to me, lol

  14. Rajini Rao says:

    That was quite a dramatic video, Roelf Renkema ! The very best wishes for your full recovery.

  15. Thank you, for your knowledge share Rajini Rao 

    Have a nice week end.

  16. Rajini Rao says:

    You’re welcome, Jose, although the best part as usual is the image which is not mine 😉

  17. Pam Adger says:

    Roelf Renkema and Rajini Rao here is an informational video about hep C with details of the disease. 

    Hepatitis C Made Easy

  18. Murali Adari says:

    Are there going to be complications if the RBC production count goes beyond 45%. I would imagine the increased volume and its associated circulation plus the acceleration required to replace the dying cells all can add to some hyperactivity leading to some unexpected consequences ?

  19. Rajini Rao says:

    That’s a great question, Murali Adari . Blood count is measure by a term known as hematocrit. If the hematocrit is low, it could be a sign of hemorrhage. On the other hand, if it is abnormally high, it could indicate blood doping (by athletes), dehydration or diseases like dengue fever. A high blood count is usually a symptom of some underlying change, rather than a problem in itself. There’s more here:

  20. Murali Adari says:

    Thank you Rajini Rao .

  21. Chad Haney says:

    I’m great, how are you?

  22. It never fails that on the blood unit, when we talk about disorders such as these, that students want to look at their blood under the microscope.  Something easy to do the day we take blood samples to test for ABO blood types.   I love photos of the cells like the one posted here, but they really do not represent well with a standard student microscope.   I wonder if the oddly shaped sickle cells could be identified at 400x?

  23. Rajini Rao says:

    Shannan Muskopf , your students should be able to diagnose sickle cells using their phone cameras! There’s even a paper on this:

    You do need to find some carriers or patients. Perhaps a local teaching hospital or university could help. It would be so neat to have students diagnose blood samples!

  24. Rajini Rao says:

    Roelf Renkema , yes, the sickle cell mutation is common in ethnic groups that are from Africa, SE Asia and middle east, where malaria is prevalent. 

  25. I vaguely remember having read that sickle cell diseases provides some tolerance to malaria. “circulate about once in 20 seconds”, that is the time for a blood cell to be transported through a complete circle of one’s blood vessels?

  26. Rajini Rao says:

    Yes, that’s right about the estimated circulation time Dirk Schweitzer . It varies depending on the heart rate (at rest vs. exercise) and blood volume (proportional to the size of the person). The heart pumps 4-5 liters per minute. Most estimates are under one minute.

  27. Interesting, so malaria might’ve turned a genetic defect into an asset for natural selection?

  28. Rajini Rao says:

    Kevin Marshall , that’s right! Otherwise, as a harmful mutation, it should have just dropped out of the population due to natural selection. The question is, how will the frequency change if malaria is eradicated in the future, while at the same time, treatments for sickle cell anemia prolong patients lives? These are opposing pressures that may influence the frequency of the mutation.

  29. Rajini Rao says:

    Excellent collection of papers, thanks for the link Dirk Schweitzer .

  30. awesome summary Rajini Rao thanks to you and Chad for educating us…

  31. Rajini Rao says:

    You’re too kind, John, and it’s my pleasure. 

  32. Thanks Rajini Rao… That was mind expanding ! … I was won ring if you could explain what’s going on with the blood of someone having haemophilia

  33. Rajini Rao says:

    Pradeep Mathew ,  hemophilia is a blood clotting disorder. It can be life threatening if the bleeding is internal and cannot be stopped. It is inherited and affects only males (“sex-linked”) is caused by mutations in clotting factors. In addition to the red blood cells shown here, there are even smaller cells called platelets that can aggregate at a wound site to form a clot. The signal to aggregate comes from the clotting factors.

  34. Rajini Rao says:

    Happens to all of us, Dennis Bennett 😀

  35. Drdilip Soni says:

    truth and fate of negative change …….. harm

  36. Laith Salem says:

    thanks for the post.magical 

  37. good introduce of erythrocyte

  38. Rajini Rao says:

    “Landolina, a 20-year-old junior at New York University, created a gel from plant polymers that mimics the human extracellular matrix, a substance produced by the body that sets off the process of blood clot formation. He calls it Veti-Gel.” Apparently, this stuff seals wounds in seconds. There are other products made by DARPA and the US military that are being used to quickly seal and heal interesting read!

    Stop Bleeding Instantly!

  39. A knowledgeable and learnable article.  

  40. Una foto peculiar y diferente.

  41. James Clear says:

    nice post..very informative Rajini..

  42. Indeed I remember this correlation with sickle-cell and malaria resistance, but what is the clinical and physiological meaning. Lets say 1 parasite infects 1 rbc, does it survive? is it statistical? Wonderful post and mightily thought provoking.

  43. Rajini Rao says:

    chaitanya athale , an equally thought provoking question 🙂

    Infected red cells don’t survive; in any case, red cells have a short life span. More importantly, the parasite interferes with the ability of the red blood cell to carry oxygen, its most important function. A person with some population of red cells in the sickle form will be partly resistant to the malarial parasite because of the difficulty the parasite has in infecting the sickled cells. So this person fares better, over all, from the infection.

  44. what is the mystery that only WBC are concerned with disease resistance? I said this b/c sicled RBC also resist malaria infection


  45. Thank you very much for add me to your circle and thank you for providing this information for those who know this world, but surely serve scientists to find solutions to certain diseases, so congratulations though I did not understand.

    Best regards.

  46. Rajini Rao the sickle cell / malaria example is the classic one we always learn to illustrate this phenomenon.  i always wondered: what is the next best example?

  47. Rajini Rao says:

    nomad dimitri  The other commonly cited example of heterozygous advantage is cystic fibrosis. One in ~25 people of European descent is a carrier, which is pretty high considering how deadly the disease can be (especially in the past, where no treatment was available to prolong life). There are a couple of theories for this. One, that heterozygous people are more resistant to cholera (cholera toxin activates chloride secretion by the CF protein and causes huge water loss). The second idea is that there is carrier resistance to tuberculosis, thought to be because of lower activity of a particular enzyme in CF patients, that the Mycobacterium requires to flourish.

  48. Rajini Rao that is very interesting, thank you, i had no idea!  funny that in both theories, the “protection” is against diseases that are now rare, so the advantage is eroding.  who knows what the time frame is for that to filter down to the cystic fibrosis mutation…

  49. Rajini Rao says:

    nomad dimitri , on the other hand, people with sickle cell anemia and cystic fibrosis are living longer thanks to new therapies, and have the opportunity to pass the mutation on to future generations!  This makes the evolutionary equation more complex.

  50. Rajini Rao exactly!  the ingenuity behind studies that try to unravel the causations is extraordinary.

    (btw: i was not notified on your reply from april!  unbelievable.  but i was notified when the other person commented AFTER your comment!)

    This makes the G+ communication equation also more complex.

  51. Rajini Rao says:

    Both evolution and G+ work in mysterious ways 🙂

  52. Are you saying God does play dice with G+ ?  < winking >

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