Have you thanked your thyroid today? If not, you should because your thyroid is essential for many of life’s daily activities and processes that you probably take for granted.
You can thank your thyroid for things like regulating your body temperature and appetite, and keeping you energetic, slim, and focused. That’s because these small glands in your neck are hormone-producing factories, and thyroid secreted hormones (TSH) control the growth and development of our organs and tissues and regulate important processes like your metabolism.
When your thyroid doesn’t work…
People who have thyroid disorders suffer from a number of uncomfortable or even nasty symptoms. Those with overactive thyroid glands (hyperthyroidism) produce too much thyroid hormone and have an overactive metabolism, which causes symptoms such as excessive sweating, weight loss, heart problems, and sensitivity to heat. Those with underactive thyroids (hypothyroidism) don’t produce enough hormone and have an impaired metabolism, which causes symptoms of tiredness, reduced heart rate, hair loss, feeling cold, and weight gain.
There are other types of thyroid problems (cancer and inflammation to name a few), but the bottom line is that, if your thyroid isn’t functioning properly, your quality of life will be negatively affected.
A stem cell-lution to hypothyroidism
However, there maybe a new “stem cell-lution” therapy for some forms of thyroid dysfunction. Scientists from the Boston University School of Medicine and the Beth Israel Deaconess Medical Center reported in Cell Stem Cell on Thursday that they can generate functional thyroid tissue from stem cells derived from different mammalian models. This is a huge deal because previously, scientists were unable to manipulate pluripotent stem cells into mature thyroid cells that had the correct thyroid identity (meaning they turned on the correct combination of thyroid-specific genes). This previous inability has made it very difficult for scientists to model thyroid diseases in a dish.
In this study, the authors used two factors, BMP and FGF, to directly differentiate mouse pluripotent stem cells into thyroid progenitor cells. These progenitors could be coaxed further into mature and properly functioning thyroid organoids (3D thyroid-like structures) that secreted thyroid hormone both in a dish and when transplanted back into mice.
What was truly exciting about their discovery, was that the same two factors could make functional thyroid tissue from mouse, frog, and human pluripotent stem cells, showing that the role of BMP4 and FGF2 in thyroid development is conserved across multiple species.
With the bases loaded, the authors hit a grand slam by using BMP4 and FGF2 to generate thyroid progenitor cells from human embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) derived from the skin cells of both healthy individuals and patients with hypothyroidism.
This study not only offers a new understanding of the early stages of thyroid development, but provides a potential source of transplantable stem-cell derived thyroid progenitor cells for cell-based therapies that could treat some forms of hypothyroidism.
In a press release from the Beth Israel Deaconess Medical Center, co-senior author of the study Anthony Hollenberg explained the significance of their findings:
This research represents an important step toward the goal of being able to better treat thyroid diseases and being able to permanently rescue thyroid function through the transplantation of a patient’s own engineered pluripotent stem cells.
Co-senior author Darrell Kotton went further to describe the novelty of their discovery:
Until now, we haven’t fully understood the natural process that underlies early thyroid development. With this paper, we’ve identified the signaling pathways in thyroid cells that regulate their differentiation, the process by which unspecialized stem cells give rise to specialized cells during early fetal development.”
Remembering Anita Kurmann
While this discovery is a major step forward in the field of thyroid disease and regenerative medicine, the victory is bittersweet in light of the recent passing of the study’s first author, Anita Kurmann. Anita was a Swiss surgeon and a talented scientist who was tragically killed while riding her bike in Boston’s Back Bay on August 7th, 2015. She had just heard that her publication would be accepted to Cell Stem Cell days before the accident and was planning to start her own lab at the end of the year in Switzerland.
Her colleagues, friends, and the science world will miss her dearly. As a tribute to Anita, her co-authors dedicated the Cell Stem Cell publication to her memory.
We dedicate this work to the memory of our co-first author, Dr. Anita Kurmann, who died in a tragic bicycle accident when this manuscript was in the final stages of formatting. She was intelligent, well read, kind, humble, and tirelessly committed to her patients, her thyroid research, her family, and her colleagues, who miss her dearly.